Case No: HQ/12/X03852
Neutral Citation Number: [2016] EWHC 351 (QB)
IN THE HIGH COURT OF JUSTICE
QUEEN'S BENCH DIVISION

Royal Courts of Justice
Strand, London, WC2A 2LL

Date: 26/02/16 

Before :

MR JUSTICE HICKINBOTTOM
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Between :

	SALLY LILLINGTON
	
Claimant	
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	(1)	GREGORY ANSELL
(2)	SIMON JENNISON	

Defendants	

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Martin Spencer QC and Tejina Mangat (instructed by BL Claims Solicitors) 
for the Claimant
Martin Porter QC (instructed by Gordons Partnership) for the Defendants

Hearing dates: 12, 13, 14, 15, 18, 19, and 21 January 2016
Further written submissions: 22 January 2016

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Judgment
Mr Justice Hickinbottom : 
Introduction
1.	Early in the morning of 29 September 2009, the Claimant Mrs Sally Lillington woke with symptoms of cystitis.  She had had this condition before, and took a prescription antibiotic tablet which she had left over from a previous episode.  Shortly afterwards, she started to feel sick, and she vomited regularly over the course of the next couple of days.  She contacted her medical practice, and had a number of telephone and face-to-face consultations with doctors from that surgery, including each of the Defendants, Dr Gregory Ansell and Dr Simon Jennison.  In the meantime, she drank substantial amounts of water, which she thought would assist with the cystitis and prevent her becoming dehydrated as a result of being sick.  
2.	By the evening of 1 October, she was still very unwell and she rang the NHS out-of-hours medical service.  In the early hours of the following morning, she received a home visit from an out-of-hours service doctor, who advised that she should be admitted to hospital.  He called for an ambulance.  However, before it arrived, the Claimant collapsed and began to fit.  
3.	She was admitted to Royal Bournemouth Hospital, where she was diagnosed as having acute dilutional hyponatraemia, i.e. low sodium concentration in the blood caused by excessive consumption of water.  The associated cerebral oedema had led to an encephalopathy, i.e. a swelling of the brain.  She was treated so that the sodium levels were quickly normalised, and the swelling reduced.  However, the Claimant has been left with enduring personality, emotional and behavioural changes.  Her primary contention is that those changes arise from frontal lobe damage caused by the hyponatraemia and consequent encephalopathy.  The Defendants do not accept that the Claimant has suffered permanent organic brain damage.
4.	Dilutional hyponatraemia is an extremely rare condition, and it is not suggested that any of the healthcare professionals who treated the Claimant ought to have foreseen it occurring in this case.  However, it is the Claimant’s case that, at the time of her consultation with each of the Defendants, her condition was such that she ought to have been admitted to hospital, at the time of the consultation or shortly thereafter.  On admission to hospital, she would inevitably have been given conventional blood tests which would very quickly have identified the low sodium level which would then have been corrected prior to any fitting or encephalopathy.  Each of the Defendants was thus negligent in not ensuring that she was admitted to hospital; and, if either had acted as he ought to have done, she would have been admitted to hospital earlier than she was, and the encephalopathy and brain damage would not have occurred.  The Defendants consider that their care of, and advice to, the Claimant was appropriate.
5.	Therefore, whilst there are a number of substantial factual disputes – including the frequency and duration of the Claimant’s vomiting, and her presentation to each of the doctors – the claim gives rise to the following key issues.
i)	Breach of duty:  Did Dr Ansell and/or Dr Jennison breach his duty of care towards the Claimant in failing to ensure that she was admitted to hospital earlier than she was in fact admitted?
ii)	Legal causation:  It is not contended that either Defendant ought reasonably to have foreseen that the Claimant would drink water in such quantities as would cause hyponatraemia.  Nevertheless, if, in the light of her presenting condition, Dr Ansell and/or Dr Jennison was in breach of duty in failing to admit the Claimant to hospital, the following issue arises: is legal causation proved if, on the balance of probabilities, the investigation to which the Claimant would have been subject if admitted would in the event have revealed a low sodium level that would have been normalised before it caused fitting, encephalopathy or any substantial brain damage or other injury?
iii)	Medical causation:  Until the closing submissions, the Claimant’s case was reliant upon proof of an enduring organic brain injury as a result of the hyponatraemia.  Consequently, if there was a breach of duty, the issue arises as to whether the Claimant’s hyponatraemia led to the brain damage which, she contends, is responsible for her continuing symptoms.  In closing, Mr Martin Spencer QC for the Claimant sought permission to re-amend to add an alternative claim based upon the proposition that the hyponatraemia caused continuing psychological symptoms alone.  There is an issue as to whether the Claimant ought to be allowed, at this stage, to re-amend to add that new claim.
iv)	Mental capacity:  As a result of an impairment of, or disturbance in the functioning of, her brain or mind, is the Claimant unable to make relevant decisions in relation (a) the conduct of this litigation and/or (b) her own financial affairs, such that she lacks capacity in respect of those matters?
v)	The amount of the claim is very much in dispute.  The Claimant values the claim at £1.6-1.8m; the Defendants value it at about £250,000.
6.	At the trial, the Claimant was represented by Mr Spencer and Ms Tejina Mangat, and the Defendant by Mr Martin Porter QC.  In addition to evidence from the Claimant and her husband, and from the Defendants, I had the benefit of considerable expert evidence.  The Claimant called the following expert witnesses: Dr Adrian Rogers (General Practitioner), Dr Solomon Almond (Consultant Physician), Dr Wellesley St Clair Forbes (Consultant Neuroradiologist), Professor David Chadwick (Consultant Neurologist), Dr Nicholas Leng (Consultant Clinical Neuropsychologist), Dr Paul Shotbolt (Consultant Neuropsychiatrist) and Mr Jon Mavers (Physiotherapist and Care Expert).  The Defendants called the following experts: Dr Naz Pambakian (General Practitioner), Dr Shawn Halpin (Consultant Radiologist), Dr Michael Nelson (Consultant Neuroradiologist), Dr James Ahlquist (Consultant Physician & Endocrinologist), Dr Robin Howard (Consultant Neurologist), Dr Laura Bach (Clinical Neuropsychologist), Dr Michael Isaac (Consultant Psychiatrist) and Ms Justine Fawcitt (Occupational Therapist and Care Expert).
Hyponatraemia
7.	Sodium is essential for the functioning of the human body, notably in the regulation of the amount of water in the body, and thus blood volume and pressure.  The transmission of sodium at a cellular level is also vital for the proper functioning of a variety of processes, including those of the brain, nervous system and muscles.  
8.	The normal range of sodium concentration in the blood (“the serum sodium level”) is 135-145 millimoles per litre (mmol/L).  Hyponatraemia occurs when the serum sodium level is below that range.  It is termed “severe” if the level falls below 125 mmol/L.  “Chronic hyponatraemia” occurs when the sodium level drops gradually, often over several days or weeks, e.g. as a result of an underlying condition such as congestive heart disease.  “Acute hyponatraemia” is defined as that occurring over a period of 48 hours or less, and is caused by the rapid dilution of sodium by expulsion of sodium from the body in greater quantities than its intake, e.g. by the intake of very large amounts of fluids with low levels of sodium including water over a relatively short period of time (polydipsia), or the replacement of salt-rich sweat with pure water under certain circumstances such as those of a marathon runner. 
9.	Very low levels of serum sodium may cause cerebral oedema and associated encephalopathy: water is retained in the cells of the brain causing swelling and thus an increase in pressure within the cerebral cavity.  Severe hyponatraemia and hyponatraemic encephalopathy are associated with a variety of symptoms, including vomiting, nausea and headaches.  Although, in general terms, there is an adverse correlation between the level of sodium and symptomatology, the presence and course of such symptoms is very variable.   Furthermore, as the pressure in and around the brain increases, there is a risk of substantial damage by way of cerebral herniation or as a result of a consequent adverse impact on the flow of oxygen (hypoxia) and/or blood supply (ischaemia) to the brain.  There is also a risk of serious injury from the over-rapid correction of hyponatraemia, which may cause the breakdown of nerve cell sheaths (central pontine myelinolysis (“CPM”)), a potentially devastating condition which appears to be restricted to the normalisation of hyponatraemia in the chronic form.  
10.	Where the cause of acute hyponatraemia is simple, its treatment may be confined to removing that cause: for example, in a case of polydipsia, if the patient stops drinking extreme amounts of low sodium fluids, the body will very quickly self-adjust – the body will retain sodium, and rapidly expel large amounts of low-sodium urine – without the risk of CPM.  However, in appropriate cases, treatment may also include (e.g.) intravenous sodium fluid.
The Claimant’s Medical Background
11.	The Claimant was born on 17 February 1953.
12.	Her early medical records are difficult to decipher; but, in early 1978 (when she was 25 years old), she seems to have attended her GP complaining of “chest aches”, which was the subject of investigation including more than one echocardiogram which ultimately proved negative.  She appears to have been prescribed diazepam (an anxiolytic) at or about this time, and she continued to take diazepam continuously until about 1984.  During this period, there are a number of references to symptoms being associated with particular stressors, e.g. in January 1980 there is a reference to “tiredness, tension upper chest sensation”, and the fact that she “has had minor episodes since Sept each self-limiting”, with the suggestion that the then-current episode might be associated with “moving house”.  In March 1980, there are references to “tiredness”, “nausea”, “aching” and, specifically, “headache and tension”.  From the medical records that are legible, these appear to have been episodic and, until the mid-1980s, none of the episodes appears to have lasted for very long.
13.	During 1980s, the Claimant’s first marriage became increasingly difficult and stressful.  In the period 1984 to 1986, she received psychological assistance in the form of counselling; and there is a reference to the Claimant and her first husband both perceiving her as “the ‘sick’ partner”.  The Claimant was divorced in 1991.  
14.	At the very end of 1993, she contracted myalgic encephalomyelitis or chronic fatigue syndrome (“CFS”), and she was poorly for some time.  There are references in the medical records for July 1995 to “tired++” and “tired all time, low backache”, but such references peter out by 1996.  The Claimant says, and I accept, that she recovered from this substantial episode of CFS by 1996.  In the meantime, the Claimant met and, in November 1995, married her second husband, Mr Simon Lillington.
15.	The evidence of the Claimant and her husband, as reflected in her medical records, is that the Claimant generally enjoyed good health for the period from 1996 to 2008.  She continued to suffer from cystitis regularly; but she had relatively little by way of recurrence of psychological symptoms.  There appear to be only two episodes for which she sought medical assistance.  First, on 20 January 2003, there is a GP note:
“ ‘Post viral’ non-specific aches and pains.  Feels tired.  Viral illness over Xmas.  Slight thoracic backache tender over muscles.  
Imp[ression] Non-specific aches & pains.  
Plan Review if not settling.”
It seems to have settled relatively quickly: there is no further note in relation to that episode.  Second, in October 2006, there is the following note:
“History: Start of September family visited from Australia.  Viral type illness – temp cough, general fatigue.  Now resolved but has been left feeling very tired.  Normal activity in the morning, sleeps in the afternoon for a few hours, then sleeps all night.  Doesn’t wake feeling refreshed.  Appetite good.  Lost ½ stone over 3 weeks.  Bowels – bit constipated.  No blood or mucus.  Had a similar episode in the past (?1994) recovered but often finds if pushes too hard – very tired for next few days.  Enjoying life…
Comment: Likely post viral.  Check bloods to exclude physical cause.”
These tests were conducted, and were apparently negative: in the records, there is no follow up entry after the test results had been presented.
16.	In September 2008, the Claimant was stung by a wasp, and had a severe adverse reaction.  As a result, she requested and obtained desensitisation from wasp anaphylaxis.  It is not clear precisely when that occurred, but there are two separate GP notes dated 21 July 2009, suggesting that the Claimant’s CFS symptoms recurred as a result of her “overdoing it” as well as her wasp venom desensitisation: 
“Desensitisation brought ME back with a vengeance.”
“History:  has ME, overdid it last week, today feeling really ill – sore throat, fever – getting hotter.  No aches and pains no cough no diarrhoea. Poss onset of cystitis symptoms.  No vomiting, eating OK.”
She appears to have been prescribed nitrofurantoin, an antibiotic used in the treatment of cystitis.  There is no recorded follow up. 
17.	Before the events of September/October 2009, the Claimant and her husband describe her as a person who lived an active and full life, with which her health did not interfere.  She was industrious, looking after several properties which they let out including a holiday cottage in the grounds of their own property.  She looked after their home and extensive garden, about which she was particular, and did all of the shopping, cooking etc, and her fair share of household administration.  She did the decorating and DIY jobs around the house.  She had in the past bred show cats, with some success; and she still owned cats and trained dogs.  They kept chickens, which she looked after.  In addition, she had a full social life, for example regularly playing badminton, doing yoga and meeting friends.  
18.	Without diminishing the potential importance of the episodes of ill-health I have described, I broadly accept that portrayal of the Claimant’s life before the index events.
The Index Events
19.	The events particularly relevant to this claim took place in a period of about 5-6 weeks from 29 September 2009.  The Claimant cannot recall anything from 29 September until about 2 November 2009, when she can remember being in hospital.  The evidence in respect of this vital period therefore comes from her husband and various healthcare professionals involved with her treatment, and her medical records.  The record of telephone calls made from the Claimant’s home assists, at least with the timing of some events.  
20.	At about 06.30 on 29 September 2009, the Claimant awoke with severe symptoms of cystitis.  She had some nitrofurantoin tablets left from a previous episode; and she took one.  Within a short time, she felt sick and vomited.  Her husband says that she “continued to vomit every 20-30 minutes or so”: although he did not enter the en suite bathroom where his wife was being ill – the bathroom was small, and she understandably wanted her own privacy – he said that there was no door to it, and he could see and hear her vomiting.  She was sick a couple of times before he left for work.  
21.	At 09.24, the Claimant telephoned her doctor’s surgery (Cornerways Medical Centre, Ringwood), to make an appointment.  Because her illness had so quickly followed her ingestion of the antibiotic tablet, she told the surgery that she thought it was a reaction to that medication.  The Claimant had two consultations with Dr Clive Shaw that day.  It seems that the records for those two events may have been elided in the main note; although whether certain advice was given in the morning or afternoon is of no real moment.  At 09.40, the Claimant either attended the surgery or (more likely) spoke to Dr Shaw on the telephone.  He appears then to have prescribed Cefaclor, another antibiotic used in the treatment of cystitis.   The Claimant rang the surgery again at 13.36 and 15.15, attending the surgery shortly afterwards (recorded as 15.20), when she saw Dr Shaw.  The notes say that the Claimant presented with “vomiting on econashia”, possibly a reference to “echinacea”, a herb widely used as an alternative medicine for the treatment of infections.  The Claimant (who indicated she was generally willing to try “good” alternative medicines, and used an alternative medical practice in Winchester as well as her general practice surgery) said that she had tried to grow echinacea at one stage, but had never used it and indeed had never had it in the house; evidence supported by her husband.  In addition to the Cefaclor, the doctor prescribed oral prochlorazepine malleate (“Buccastem” or “Stemetil”, a phenothiazine dopamine receptor antagonist, used for the treatment of nausea and vomiting).  However, it seems from later evidence that the Claimant never took the antiemitic then prescribed; and, indeed, never had the prescription made up.  
22.	When Mr Lillington got back from work in the late afternoon that day, he said his wife was still vomiting continuously every 20 minutes or so; and she was also still suffering from symptoms of cystitis.  She was drinking lots of water “because she was going to the toilet frequently as well as vomiting regularly”.  She had a jug of water in the bathroom, which she would drink every time she was sick or passed urine.  She did not mention having a headache.  Because his wife was ill, Mr Lillington slept in the spare room that night; but he said he could hear his wife getting up and vomiting regularly throughout the night.  He had never known anyone being sick so frequently.  The Claimant did not tell him that she had been prescribed antiemetics: if she had, he said he would have collected the prescription for her, although, as his wife believed the illness was due to an adverse reaction to drugs, he thought she would have been reluctant to take any further drugs “unless absolutely necessary”.  
23.	In any event, Mr Lillington said that, the following morning (Wednesday 30 September 2009), the Claimant was no better; and she continued to vomit every 20-30 minutes or so.  She also complained of a severe headache.  Mr Lillington however considered his wife was in control of matters, and he went to work as usual.  
24.	That day, the Claimant had two further telephone consultations with different doctors at the medical centre.  First, at 13.30 she spoke with Dr Yvonne Denman.  The notes record:
“Comment: nitrofurantoin caused sickness and headache, cystitis improving, no tummy pain bowel sl diarrhoea only hasn’t used stemetil and doesn’t want to says no fever, gen adv re hydration. I would expect sitn to be much improved by tomorrow”.
I mark the reference there to the Claimant having reported “headache”, something to which I shall return.
25.	Then, at 17.35, apparently prior to her husband’s return, the Claimant telephoned the surgery again, and spoke with Dr Jeni Worden.  The notes record:
“History: telephone encounter re alleged side effects of nitrofurantoin, insists not infection, she has no doubt it is a reaction, very resistant, says has not collected prescription from chemist for Buccastem but also feels very sick, lots of worries about health, advised that she has to decide what to do but my advice would be to take the cephalexin if the cystitis is getting worse and the Buccastem if the sickness persists…”.
26.	Mr Lillington returned home in the late afternoon, when (he said) the Claimant “looked awful” and said she felt extremely ill.  He said she told him that she “had the worst headache that she had ever had”.  She continued to vomit regularly; and continued to drink water which (she told him) the doctors had advised her to do.  He said that, again, he slept in the spare room; but heard his wife get up in the night “regularly to vomit”.    
27.	The following morning (Thursday 1 October 2009), the third day of the Claimant’s illness, Mr Lillington said his wife was no better, although she did not complain to him of a headache that day.  He observed her vomiting every 20-30 minutes.  However, he considered his wife still had matters under control, and that she would contact the surgery again if she believed that was necessary.  She could also call him.  He thus went to work in the morning, as usual.
28.	However, the Claimant called the surgery at 09.59, in a call which lasted over nine minutes.  Although Dr Ansell – the doctor on duty call – initially recalled that he had been asked by the receptionist who took the initial call to telephone the Claimant back and he did so, from this entry it seems more likely that the receptionist put the initial call through to Dr Ansell.  He said that, in any event, he would have had recourse to the computerised medical records, to which he could refer on screen whilst speaking to a patient on the telephone.  He considered that the Claimant should be seen, as a result of her continued cystitis and vomiting, and her concern about her own condition.  Furthermore, he said he was concerned by the reference to “headache” he had seen in Dr Denman’s note, which diagnotistically brought into play a number of serious conditions as possibilities.  As the Claimant said she could not get to the surgery, a home visit for later that day was arranged.  The medical record does not note anything further from that conversation: it simply records:
“History: phoned, needs visit.”
29.	Dr Ansell made that visit, later that morning.  He said that he arrived at about noon, and was there until about 12.45 when he left to ensure that the mid-stream urine (“MSU”) sample he had taken would be sent on for tests that day, the samples leaving the surgery at about.  However, he had back-calculated those times from the time he must have returned to the surgery to ensure that the sample was sent off for analysis; and, as the Claimant is recorded making a half-minute telephone call from home (to an alternative medicine practice in Winchester) at 12.25 that day, it seems likely that Dr Ansell had left by then.  His visit probably lasted about 20-30 minutes.
30.	Dr Ansell said that he remembered the visit well.  In his evidence, he said that, prior to his attendance, he had considered all of the relevant computer medical record entries.  From those and his earlier conversation with the Claimant, he expected to find someone significantly unwell; but, when he arrived at the Claimant’s house, the door was unlocked – unsurprising in this country area – and he walked in to find her up and dressed.  She was not distressed, and did not appear to be ill: she was talking sensibly, and did not appear to be dehydrated.  There were no signs that she had been recently vomiting.  He said that she told him she had had symptoms of cystitis and some nausea and vomiting since 29 September; the vomiting had persisted, being frequent on the Tuesday and Wednesday of that week, but less severe that morning when she had vomited twice since 08.00 or (more likely) 09.00.  He said that the Claimant told him, in terms, that she was better than she had been the previous two days.  She did not spontaneously refer to headache at all.  However, in his statement, Dr Ansell said that, in response to direct questioning, she told him that she had had a mild headache which began after the vomiting had started.  In cross-examination, he said that he thought she had said she still had a headache when he saw her.  It had been worse the previous day (Wednesday), but had improved.  It was persistent, but mild.  She had taken no medication for it.  She said that she had taken neither the antibiotics nor the antiemetic medication which had been prescribed to her the previous day.  Dr Ansell said that she told him she had taken echinacea through her current illness.  He examined her and found no gross behavioural or central nervous system abnormalities.  There were no abnormalities in the eye movement range and pupil reaction to light, or in her neck movement.  There were no signs of dehydration, although the Claimant’s throat was red suggesting a throat infection or possibly recent vomiting.  A dipstick urine test suggested evidence of a possible infection, but was otherwise normal, there being no presence of glucose or ketones.
31.	Dr Ansell said that the Claimant thus showed no signs of any serious provocative illness or dehydration.  He strongly suspected a urinary tract infection (“UTI”), which may have migrated upwards; but he accepted that nitrofurantoin might have been the cause, given that nausea and vomiting are well-known side-effects of that drug.  
32.	Having excluded serious pathologies, he advised the Claimant to have an antiemetic to control her symptoms of vomiting; and that initially this could be by way of injection.  She indicated that she did not want an injection; but, Dr Ansell said, she agreed to take Buccastem in oral form which, absent an injection, he “strongly recommended”.  He said he gave her two tablets, one of which (he said) she took immediately and in his presence.  He left the other to be taken in 2-3 hours time, if the symptoms persisted.  He also advised her to maintain regular fluid intake to replace what was being lost through vomiting and, whilst such fluids could include water, a Dioralyte or equivalent electrolyte powder made up with water, or a home-made preparation of water and salt, would be a better alternative.  
33.	Dr Ansell said that he would review her condition and progress the following day, either at home or at the surgery, by when the MSU analysis ought to be available.  In the meantime, he said he would speak to his colleague Dr Jennison, who was due to take over from him as duty doctor in the afternoon, so that he would be aware of her situation – and that she should contact him if her condition continued or worsened in any way.
34.	That was Dr Ansell’s evidence.  His notes of the home visit were short.  They record:
“History: contd vomiting and cystitis
History: hasn’t taken Buccastem
Examination: afebrile, abdo nad, blood and leucos on dipstix 
Examination: red throat
Comment: diagn unclear, no pre event msu, she thinks nitro and/or cef responsible, but ? viral vomiting 
Comment: redo msu and start buccastem (declined inj).  Rv tomorrow”
35.	When Dr Ansell left the Claimant’s home, he returned to the surgery where he bagged up the MSU sample, which left the surgery for analysis at about 13.00.  
36.	Dr Ansell then attempted to speak to Dr Jennison, eventually making contact by telephone at about 15.00.  Dr Ansell said he explained that the Claimant appeared to have an unresolved UTI, although her symptoms appeared to be improving.  An MSU analysis was awaited.  He said he also explained to Dr Jennison that he had administered an oral antiemetic, and planned to review her the following day unless her condition worsened at which point she would contact him.  Dr Jennison recalled that conversation – but did not recall Dr Ansell mentioning having administered any antiemetic to the Claimant.  
37.	At 17.34, the Claimant telephoned the surgery again, and spoke with Dr Jennison who was by then on duty.  In his evidence, Dr Jennison said that, despite it being late afternoon and what appeared to have been good advice from his colleagues (including Dr Ansell), he thought that “this patient was still not right”.  His note reads:
“History: feels ‘awful still’ vomiting lots and cystitis sx
Comment: come down and examine again ?ascending UTI check glucose 
Medication: Domperidone Suppositories 30 mg 10 suppository  ONE PR  PRN”.
The reference to domperidone (“Motilium”), another dopamine receptor antagonist used as an antiemetic, is not entirely clear; it does not appear to have been a prescription made over the telephone, and may have simply have been a reference to the antiemetic that had already been prescribed.  In any event, during that telephone call, Dr Jennison told the Claimant that he had better facilities to examine her at the surgery, and asked her to attend there before 18.30 when they closed.  She said she would do so.  Whilst he waited for her, he read through the notes of her recent contact with those at the surgery.
38.	Mr Lillington had by this time arrived home, and the Claimant told him she had seen a doctor but still felt terrible, so had made an appointment to go to the surgery.  He drove her there, but did not go in with her.  He stayed in the car.
39.	She saw Dr Jennison at 18.11.  Dr Jennison said that she did not look particularly unwell, although she appeared anxious.  There were no signs of her having recently vomited, and she did not (e.g.) have a bowl with her.  Her main concerns were nausea (rather than vomiting) and anxiety about what she presumed to be sensitivity to the antibiotic she had taken.  He said that he was sure she did not say that she had vomited every 20-30 minutes – because he would have recorded that as something exceptional, but he made no record of the frequency of vomiting at all.  He did not refer to headaches in his statement; but, in cross-examination, he said he knew from the records that she had had a headache – the reference in Dr Denman’s note from the previous day – and that he asked the Claimant whether she had (or had had) a headache, and she said she had not.  
40.	Dr Jennison examined the Claimant, including performing a blood sugar test which was normal, and a full cranial nerve examination which had the same finding as the earlier examination by Dr Ansell noted by Dr Jennison as “PERLA”, i.e. “pupils equal and reacting to light and accommodation”.  That examination, he considered, ruled out diabetes and a neurological cause for the Claimant’s problems.  His working diagnosis (he said) lay between viral gastritis and incompletely treated cystitis, complicated by nausea, possibly as a result of sensitivity to nitrofurantoin.  There was nothing to suggest any serious underlying pathology.
41.	The Claimant led Dr Jennison to believe that she had not taken any antiemetic medication.  Dr Jennison said that the Claimant was “absolutely clear” that she did not want any suppositories; but she agreed to an injection of metoclopramide (“Maxalon”, another antiemetic dopamine antagonist) which Dr Jennison administered.  The Claimant went to her car, where she waited with her husband for 15 minutes, to see whether there was any adverse reaction to the injection.  There was not; and she went back into the surgery to see Dr Jennison.  He said that she had not vomited during her time at the surgery – nearly an hour – and, although her primary complaint was nausea, she did not appear to be unduly nauseous.  He said that, before she left, he gave her “safety-netting advice”, namely that, if she worsened or had any concerns overnight, she should call the out-of-hours service or go to A&E at the hospital.  He told her that the out-of-hours service telephone number was available on the surgery’s answer-phone.  In the meantime, he transferred the proposed review the following day from Dr Ansell to himself.
42.	Dr Jennison’s note for that day in the Claimant’s medical records reads:
“History: seen 15 mins after – no drug reaction injection
Examination: NB worse lying flat – I suspect all triggered gastritis hence PPI 
Comment: review tom am also – start cefalexin if nausea better controlled”.
Examination: T35.8 c, abdo soft non tender P 96 reg, RR 14, alert PERLA BM 5.8. 
Comment: IM Maxalon 10 mg given"
Medication: Metaclopramide Hydrochloride Injection 10 mg/2 ml ampoule 5 ampoule GIVEN BY DOCTOR 
Medication: Cefalexin Capsules 500 mg 21 capsule ONE TO BE TAKEN THREE TIMES A DAY.”
Those entries do not appear to be in chronological order.  The only “history” recorded (which is at the beginning) clearly refers to the Claimant not having any adverse reaction to the antiemetic injection (to which reference is made later in the note).
43.	The Claimant returned home, where she must have arrived at just after 19.00.  Mr Lillington said that they did not stop to have any prescription made up.  The Claimant does not appear to have vomited at all during her period away from the house; but, Mr Lillington said, she was vomiting again “within a few minutes” of her return, the injection having had no effect at all so far as he could see.  Mr Lillington said that his wife got “a lot worse” that evening.  She stayed in the bedroom alone; but, he said, he heard her vomiting frequently and he heard her call what he believed to be the out-of-hours service.
44.	We know from the telephone records that the Claimant telephoned her own surgery number twice, at 21.25 and 21.27, from which she presumably obtained the out-of-hours service number which she telephoned at 21.46.  
45.	From the Claimant’s call to that service, there are two separate, but consistent, triage notes.  The fuller reads as follows:
“Triage details:
Diagnosis:
Has a UTI has been vomiting 3 days GP gave her Injection at 18:30 this evening to stop vomiting now feeling nausea.  Was taking nitrofurantoin which has been stopped started on Cephalexin not taken yet as nauseous.  TAS Recommends: NONE Recommend Self-Care Triage Change Reason: pt requesting GP…  Questions:  Is the patient home alone?: No.     Symptoms: feels very sick and has meds that makes her feel very faint.  Comments:  seemed reluctant to tell me anything other than that.  Presenting complaint: Nausea. Odyssey Recommends Self-care Richardg upgraded from No Urgency to Less Urgent Assessment Variance: pt requesting GP.”
The Claimant’s primary complaint was therefore recorded as nausea; and there is no reference at all to headache.  At 21.56, after triage assessment, the priority for the call was set to “routine”.
46.	At 02.13, no doctor having yet attended, the Claimant called the out-of-hours service.  We have the benefit of a transcript of this, and of the later calls with the same service.  Mr Lillington was not a party to the calls: the Claimant instigated and conducted them herself.  This first call – and the other conversations between the Claimant and the out-of-hours service – are particularly important, given the Claimant’s amnesia in respect of the relevant period, because these are conversations, of which we have an accurate transcript, between the Claimant herself and a healthcare professional shortly before her collapse and period of amnesia.  
47.	The general gist of the first conversation was that the Claimant was “feeling sick… really sick… not just sick, really bad” – and was anxious for the out-of-hours doctor to arrive and for any advice in the meantime.  The Claimant said that the doctor had given her suppositories “for feeling sick”.  The initial call handler probed this a little, as recorded in the transcript:
“Ambulance service: … And you are feeling sick at the moment are you?
Claimant:  Oh really bad.  Not just sick, really bad.
Ambulance service: Okay.  Can you…
Claimant:  I’ve had a reaction I think to some antibiotics or something.
…
Ambulance service: … Are you bleeding or vomiting blood?
Claimant:  I… I was a little bit, earlier.
Ambulance service: Okay, when do you call…
Claimant:  Blood.
Ambulance service: … when are you saying earlier.
Claimant:  Oh, about…
Ambulance service: How long ago?
Claimant:  Er, about two hours.  Two or three hours. [Sigh]  Oh God.
Ambulance service: Okay.  How much blood was in your vomit love?
Claimant:  Not much.
Ambulance service: Okay…”.
48.	The call handler then put the Claimant through to a nurse, who confirmed that the out-of-hours doctor was on the way, and should be with the Claimant very shortly.  The Claimant said she had not taken the suppositories, as the nausea was getting worse and she was getting weaker.  The nurse continued:
“Nurse:  And, er, have you vomited?
Claimant:  A – well, a little bit?
Nurse:  Okay.  And what, just the once?
Claimant:  Yes.
Nurse:  Any diarrhoea?
Claimant:  No.
Nurse:  Any pain anywhere?
Claimant:  I just feel terrible.  Really, really bad.
Nurse:  Okay.  Any pain anywhere?
Claimant:  No.  Well, in the middle of my chest… a little bit.
Nurse:  Right.  So you have got pain… You said no, then you said yes.  So have you got pain at the moment?
Claimant:  I only feel I’m going to be sick.
Nurse:  Okay. So, and, erm, are you otherwise normally fit and well?
Claimant:  Well, I do suffer with… yes… I’ve got ME.
Nurse:  Yes.
Claimant:  But generally it’s not too bad.
…
Nurse:  … [T]ell me exactly in what way you’re feeling terrible.  
Claimant:  Erm… very, very sick and very… faint.  Very, very sick.
Nurse:  Right, so it’s the main feeling of nausea that’s… that’s the problem?
Claimant:  Oh very sick.  Very sick.  Not… I’m much worse than I’ve ever been.  I’m not exaggerating…”.
49.	The call then ended; but the nurse telephoned back at 02.26 to say that the doctor was on his way – but, if matters got any worse in the meantime, the Claimant could always ring the out-of-hours service again.
50.	The doctor had still not arrived by 02.45, when the Claimant rang the out-of-hours service again and spoke to another initial call-handler.  She said it was getting worse.  She said that the nitrofurantoin had made her sick, but it was now “much, much worse”.  When asked to elaborate – “What’s worse?” – she said:
“Oh, the feeling of sick and… and really bad.  I’ve never felt this bad… I’ve never had feeling sick like it.”
51.	The out-of-hours doctor, Dr Sanjeev Bajaj, arrived at the Claimant’s home at 02.50.  His note records:
““History: husband is with pt – pt has been vomiting for 3 days – feels shivery/cold/light-headed/dysuria with increased urinary frequency initially – now passing less urine and still has persisting suprapubic area pain – was started on nitrofurantoin 50mgs qds – took two tabs then stopped these – own GP visited pt in the evening and gave an antiemetic injn = patient has tried stemetil/motilium – as well no help – says vomitus has been brown/sometimes pink – pt was given script for cefalexin 500mgs tds by own GP to start taking these from next day – on no regular treatment. P/H [past history] – ME, bowels have moved slightly hard stools – no melena.
Examination: appears shaky/anxious/looks pale and slightly clammy tongue appears dry cvs/chest – nad p/a [per abdomen] tender over suprapubic area slightly distended abdo bs [bowel sounds] + bp 110/60 hr – 88
Diagnosis: uti on treatment/dehydrated
Treatment: admit bmth general – c/o medics – amb [ambulance] is being arranged as urgent by bmth bed service.”
Dr Bajaj did not record anything about headache; because, the Claimant’s husband said, the doctor did not ask about headache, and neither the Claimant nor he (Mr Lillington) mentioned it.  
52.	Having arranged for an ambulance to attend to take the Claimant to the Royal Bournemouth Hospital at 03.12, Mr Bajaj left at about 03.15.  However, within a few minutes, Mr Lillington said that he heard his wife go into the bathroom again.  He went in behind her.  As she leaned over the toilet bowl and started to vomit, she made a guttural noise, collapsed and began to fit.   Mr Lillington called 999, and was told that an ambulance was already on it way.  A first responder arrived, followed by Dr Bajaj who returned at 03.53.
53.	Dr Bajaj’s note of that second visit reads:
“Symptoms: call received from Ellena at ambulance control - needs dr to assist as pt is fitting and dr nearby - we agreed to attend as emergency visit with ecp on way and 999 ambulance to follow asap.…
History: had just finished seeing the pt and we got a call for us to attend as pt had had a ? fit - when we arrived the ambulance first responder was there and I found the patient sitting on the toilet floor - was rousable and mumbling words which we could not understand - appeared to be intermittently agitated and confused - apparently pt had gone to the toilet and vomited and then ? had a fit /husband not sure if any head injury was sustained - also when ambulance crew arrived husband mentioned that the pt had a very severe headache 2-3 days ago and this lasted 2 days and vomiting started soon after.
Examination: pt appeared to be agitated and intermittently confused - pupils were normal size and reactive no rash seen breathing was fast intermittently....”
54.	His handwritten Hospital Admission Form clearly has parts written from his first visit, and parts added after his second visit.  The first part includes:
“Current problem: Pt has been unwell for 3 days with persisting vomiting - frequent episodes & vomits brown fluid + some fresh bright red blood.  Lower abdo pain.  Initial Dysuria with frequency of micturition
Past medical history:  Persistent vomiting – frequent episodes of vomiting brown fluid & some fresh bright red blood…
Pt was given Injn (Anti Emetic).  Pt has also tried suppositories (Motilium) & oral STEMITIL → no help.
Passing less urine now.  Fells weak/lightheaded & shivery.
Appears pale & slightly dehydrated.
Shakes & anxious…”
On Dr Bajaj’s return visit, he added to the form:
“Pt had the worst headache 2 days ago - started vomiting afterwards Soon after I left, pt's husband called 999 → amb.
V. confused/vague Twitchy BM = 7.7
Imp: sub arachnoid haemorrhage LOC”
55.	The ambulance arrived on the scene at 04.19, and left for the hospital at 04.58.  It arrived at the hospital at 05.17.
56.	After Dr Bajaj’s return, the Claimant’s new presentation (i.e. her collapse, fitting and neurological signs such as confusion) had led to the focus of concern changing from her nausea/vomiting per se to the possibility that she had a serious condition, probably a subarachnoid haemorrhage.  Therefore, whilst on his first visit Dr Bajaj made no reference to “headache”– Mr Lillington confirmed in his evidence that no mention of headache was made during that visit – the notes of his second visit do refer to the Claimant suffering from a headache.  
57.	The medical notes from Dr Bajaj’s return onwards have to be read in the context of a then high suspicion that the Claimant had suffered a subarachnoid haemorrhage.  A symptom, and clear marker, for that condition is a so-called “thunderclap headache”, i.e. a severe headache, caused by the rupture of the cerebral aneurysm, that reaches very high intensity within minutes or even seconds of onset.  The healthcare professionals were, from that point and no doubt out of an abundance of caution, wary of any possible symptoms which might have indicated that the Claimant was suffering from such a serious condition.  They were hampered by the fact that, at that stage, the Claimant was unable to communicate with those professionals.  Any history given to them must have come from Mr Lillington.  However, the only headache which the Claimant had reported to him was on the second day of her illness (30 September).  She then reported a severe headache, but did not suggest that it was of sudden onset.  She did not mention headache to her husband at all the following day.  Nevertheless, the notes record that the Claimant had suffered a sudden onset, thunderclap headache, some recording that it had been present over the previous five days.  It may be that, in the absence of any reliable history from the Claimant and a lack of any details about the headache she had suffered, the most clinically conservative and concerning possibility on the basis of the limited history they gleaned from Mr Lillington was recorded.   In any event, we now know that the record was not accurate in respect of the characteristics of the headache the Claimant had in fact suffered.  However, these notes, once made, were recycled by successive healthcare professionals, who had no better source of the relevant history available.
58.	Dr Bajaj’s note on his return is the first in time.  He recorded “the worst headache 2 days ago - started vomiting afterwards”.  In the record made by the ambulance crew, it said:
“Hx [history]  Complained of a sudden headache (worst she had ever had) 5/7”.
59.	The Claimant fitted (possibly twice) over about an hour at home.  She fitted twice further in the ambulance.
60.	The ambulance arrived at the hospital at 05.17.  On admission to the hospital, the Claimant was initially seen by the General Medical Consultant on duty, who recorded: 
“Hx noted.
Cystitis on Mon → saw GP → nitrofurantoin 
Then developed sudden-onset, thunderclap headache with N+V [nausea and vomiting] - lasted 24-48h before settling.  Recurrence of headache
1/7 later with 2-5 mins tonic-clonic fit CT B - no bleed
Impression/Diagnosis  SAH - High suspicion.”
61.	A Critical Care Review Form was completed shortly afterwards, by a different healthcare professional, reads (so far as it relates to headache):
“Sudden thunderclap headache on Tuesday + ? Again overnight.”
62.	Six minutes after admission, at 05.23, a blood sample was taken from the Claimant, which gave a sodium serum level reading of 105 mmol/L.  She was given saline solution intravenously.  Further samples were taken that day at 06.00 (109 mmol/L) and 14.30 (127 mmol/L); and the following day at 06.00 (136 mmol/L, i.e. within the normal range).  
63.	As the notes on admission indicate, there was a high medical suspicion and concern that the Claimant had suffered a subarachnoid haemorrhage.  A CT scan performed on 2 October ruled that out as a diagnosis; but the scan showed mild to moderate encephalopathy or swelling of the brain.  
64.	The Claimant was, on any view, extremely poorly; and remained in the intensive care unit for three days.  However, she quickly improved; and the expert neuroradiologists agreed that an MRI scan on 8 October showed that the brain swelling had by then resolved, and showed no evidence of any permanent brain injury.  She was discharged home on 13 October 2009.
65.	Unfortunately, at home, the Claimant rapidly deteriorated.  Mr Lillington describes her being completely unresponsive, “just lying in bed humming”.  On 15 October, Dr Jennison visited the Claimant at her home; examined her, finding her “confused ++”; and immediately telephoned the hospital to have her re-admitted immediately.
66.	On re-admission, she was seen by Dr James Stallard, a Consultant Psychiatrist.  His note reads:
“Not able to answer any questions coherently
-	initially refers to ‘the loo’
-	repeats this reference throughout interviews, also rhyming with ‘loo’
Able to tell me first part of her address and husband’s name but little else 
Disorientated time, place, person
Has trouble word finding
-	confabulating, perseverating
Opinion – v marked neuropsychiatric deficit
I do not think this related to depression, psychosis or any other mental illness.”
67.	She continued to suffer from the symptoms described on admission, together with general confusion, agitation, tiredness and “feeling weird” (her description), which fluctuated from day-to-day.  She became fixated on leaving the hospital, and distressed by visits from her husband and daughter, when she could not return home with them.           
68.	The Claimant recovered, and was discharged home on 16 November 2009.  
The Aftermath
69.	However, both the Claimant and her husband say that, since then, their life has been very different from that which they had before September 2009 (see paragraph 17 above).  The Claimant says that she has “found that [her] brain and body have been badly affected”.  She and her husband describe, in particular, three groups of symptoms, namely (i) headaches, (ii) lack of energy and (iii) a change in the Claimant’s personality, emotions and behaviour.  These are not, of course, mutually exclusive: indeed, there is considerable mutual association and overlap.  However, it is convenient to deal with them in turn.
70.	First, she says that she has headaches, virtually every day from waking.  She tries to pace herself, but she still has the same head pains.  Of these she says (in paragraph 12 of her statement dated 27 August 2014):
“My headache/pain comes in several different types of head pain, but it is worse when I am communicating or doing too much brain work for example trying to complete normal day to day tasks.  I then get a very weird ‘rewiring’ feeling inside my head that is difficult to describe that could start one morning and go on all day as can the other pain.  Lastly I will get a headache at the back of my head which if I do not rest becomes worse.  These psychological effects of my illness have had a dramatic effect on my social life.  I rarely go out now because socialising does affect my brain and it is painful.”
71.	When, in 2012, Mr Lillington threatened to leave her, the Claimant says (at paragraph 14 of the same statement):
“… I became very ill.  I have been divorced in the past so know it is a difficult time but I never experienced symptoms like those I had in 2012.  My brain could not cope at all, thinking of the future, what would happen to my animals etc and so I became totally debilitated by my brain.  It seemed unable to process the situation and I had to lie in bed all the time.  Simon drove me to my daughter’s house in Cheltenham but even there I was in bed unable to cope with anything without extreme pain in my head.  It was truly unbelievable how my brain was affected and it is very difficult to explain to anyone the extent of the impact on me.  I went out once with my daughter to Cheltenham and after 10 minutes thought I should call 999 because I felt so bad but I held on and she took me straight back to her house.  Some days by 4pm I was in so much pain in my head that I started crying and screaming.  The crying relieved it slightly but one day after I had returned home I ended up in A&E via ambulance as I was advised by my current GP to call 999 because I was so distraught with pain and lack of understanding from anyone about how bad I was.”
72.	As to what she is able to do now, the Claimant says (at paragraphs 18-19):
“18.	This depends every day on how my brain is.  Generally I wake up with some sort of headache which does not go away, but this can be made worse if I try to do too much…
19.	… [E]very day is different with different amounts of pain.  Socialising is very difficult and communication is painful if it goes on too long.  Some days I have what I call ‘rewiring sessions’.  My head will start hurting and feel very strange, and then I will get pains in various parts of my body.  Sometimes this will last for a few hours, sometimes all day.  It is a very unpleasant experience but I have to just go with it.  It is painful and horrid….”
73.	Mr Lillington confirms that:
“She regularly complains of headaches and the only thing that will ease the symptoms is if she goes back to bed” (paragraph 33 of his statement dated 23 February 2015).
74.	She has presented to doctors with headaches from time to time.  Indeed, on 15 December 2009 (when she was ward discharged following her discharge home), she complained of headaches, but was reassured by reference to the earlier scans.  
75.	In May 2010, she was referred back to the Endocrine Clinic, with “worsening left-sided headache/altered sensation” and “concern about recurrence”.  This (it was said) coincided with particular stressors including the illness of her husband and a minor car crash.  Dr Richardson at the clinic saw the Claimant, and reported back to Dr Jennison that examination did not reveal any neurological abnormalities, and he had talked to the Claimant about what he described as “at least two MRIs both of which were robustly normal”.  No further scan then was considered appropriate.
76.	However, the Claimant was referred to Headway Dorset on 21 January 2011, again with headaches.  They recorded:
“8 out of 10 days suffer head pain so difficulty coping. My senses + emotions are magnified. Worse recently. Find everyday stresses difficult. Any social activity takes its toll on my brain, so feel isolated without support & understanding of what is happening to my brain.  
I do try to be positive but it is over a year now & recently things seem to have got worse head pain wise.” 
77.	They referred the Claimant to Dr Ralph Gregory, a Consultant Neurologist.  He recorded that the Claimant had had a very stressful year, and had had persistent headaches since the episode, which had become worse over the previous couple of months and had been accompanied by her being emotional and tearful.  He arranged for another MRI scan to be taken, but no abnormality was found.  In the note he made, Dr Burn said that he considered she had “all the issues which are typical of people with a traumatic brain injury”, diagnosing her with:
“Brain injury following hyponatraemia and seizures
Development of a fatigue syndrome and emotional distress.”
78.	In a letter to the Claimant’s GP dated 1 April 2011, Dr Burn said:
“I am sorry that her recovery has been interrupted by further stressful events….  I emphasised that in my view much of these continuing symptoms represent a presentation of fatigue problems and emotional distress that she has experienced previously. In my view she would benefit from therapeutic support in establishing a paced increase in activity and prioritising the various demands and issues that she is facing…”.
79.	In August 2012, Dr Gregory arranged for another MRI scan, which again showed no abnormality.  He wrote:
“ …She still has difficulty coming to terms with the residual cognitive effects of her brain injury two years ago. She has had access to Headway but did not find this helpful.  She has had ongoing relationship difficulties  with her husband, which have come to a head in recent months, and this has coincided with severe head  pains, which are worse when she is lying down. It was so severe last week that she went to hospital. It is worse when she has to communicate or concentrate. …
.. We spent a long time discussion the mechanism of the type of head pains that she is experiencing and I tried to explore the reasons why she should assume that a new physical problem had developed. By her own admission she has concrete views about physical and psychological symptoms. In my view she would benefit from formal psychological help and I would be pleased to ask my colleague, Burjit Gurr , if she would be able  to see her. Given the type of headaches she is experiencing she would also benefit from non-sedating tricyclic medication. I explained how we routinely use medication of this type to help people with headaches even if they do not have depression. It was clear that she would not even consider either of these strategies unless she knew that a further brain scan was normal. I therefore proposed that we had a contract so that if the scan was normal as I expected, that she would agree to accept the further help that I have suggested.” (letter to GP dated 16 August 2012).
“This lady with severe headaches has a normal MRI brain scan as expected. .. She needs to seriously consider engaging in formal psychological help. I would also suggest that she is given a non sedating tricyclic...”. (letter to GP dated 16 August 2012).
“I was able to reassure her that her MRI brain scan was normal as expected. She was particularly concerned about the blood flow and I confirmed that both clinically and radiologically there is no suggestion of a problem in this area. We once again discussed how one sided throbbing headaches associated with cognitive dysfunction are extremely common in migraine without aura. It is not uncommon for people to experience migrainous type headaches for the first time after the sort of brain insult that she had. The situation has improved from when I last saw her.  She is still experiencing episodic headaches but they are not as persistent as they were. She is in regular contact with a psychotherapist. She is not keen on taking any regular medication for her headaches at present…”. (letter to GP dated 12 September 2012).
80.	The Claimant has continued to be reviewed by Dr Gregory from time-to-time.  He has reported, more recently, as follows:
 “.. I have not seen her for two years. She has been subject to a lot of stress recently which has made it more difficult for her to cope. Her medicolegal case regarding the hyponatraemia illness is still ongoing, and there have been a number of other factors which she did not want to discuss. She has had a recurrence of the pain in her head with intermittent light headedness and poor appetite. She also described intermittent numbness bilaterally over her face and feet. ..
.. I was pleased to reassure her that there is no suggestion of a progressive neurological problem here. I also reassured her that despite the extreme stress she is under, this is not going to cause any permanent damage to her nervous system.  I have suggested she consider taking Mirtazapine.” (letter to GP dated 24 September 2014).
“I reviewed this lady who has been feeling slightly better since she had a week away and has consequently been feeling slightly less stressed. She is now taking Amitriptyline which she is tolerating, but only at a dose of 5 mg daily.  I have recommended that she should take at least 10 mg.…
She must try to avoid factors in her life which contribute to her anxiety, but this is difficult for her, particularly with the outstanding medicolegal case which hopefully will be resolved over the next year.” (letter to GP dated 16 December 2014).
81.	Second, in addition to headaches, the Claimant says that she lacks energy, and is therefore (e.g.) often unable to do housework or work in the garden.  Mr Lillington said:
“Whereas Sally used to be the sort of person who would just get things done, now it will take her time to do anything.  If she has to make three telephone calls for example, it will take her all day and tire her out.  I am therefore responsible for all the day to day running of [the house].” (paragraph 31 of his statement dated 23 February 2015)”;
 and, in his oral evidence:
“… [T]o this day I do virtually all the shopping, cooking, a lot of work around the house and dog walking.  Mrs Lillington doesn’t do a great deal around the house.”
82.	The Claimant was referred to the Brain Injury Service Clinic in September 2010, where the focus was on her fatigue and other symptoms.  Dr Burn reported back to the Claimant’s general practitioner:
“Diagnosis
Possible hypoxaemic brain injury following hyponatraemic seizures
Emergence of fatigue syndrome with residual disinhibition and emotionalism.
…. She improved immensely in hospital from the disinhibited, confused state I found her in and it appears that her jargon dysphasia has resolved completely. However, she is distressed by residual limitations. She has continuing fatigue so that she is not able to take responsibility for the animals in their smallholding apart from checking on the chickens and occasionally walking the dogs. She has not got back to cooking meals and does most of the shopping online. She has got back to making short car journeys. She is worn out by about 4.00 pm. This is associated with a hypersensitivity to smell and sound and an intermittent pain over the left side of her head. She admits to a slight disinhibition and certainly much more emotional when exposed to television programmes. All of this hasn’t been helped by a small road accident, her husband being ill and being faced with a poacher with a gun.
Her partner is a Barrister with extensive work responsibilities so that they have had to employ a girl for 2.5 hours a day to help with the animals. They have lived in the Forest for the last 5-6 years having renovated the house. She has a great interest in animal husbandry and admits to being somewhat of a perfectionist.
There is a past history of a condition diagnosed as ME after a difficult divorce in 1994. She recovered from this sufficient to be able to walk up to 4.5 miles, although with a tendency to occasional fatigue, most recently being seen after a particular stressful episode in which she got lost in the woods earlier in 2009.
Ms Lillington was somewhat tearful during the consultation but performed well with normal verbal fluency (FAS 42) and remembering three of five items of an address.  There was no focal neurological defect.
I think she has recovered with very little brain injury related impairments, maybe some emotionalism and disinhibition. This has, however, been a considerable threat to her integrity and I think it is the desensitisation to threat that underlies her hypersensitivity and fatigue. She is vulnerable to this because of her previous episode in 1994. However, there is no reason why she shouldn’t make a recovery from this in the same way as she did previously if afforded appropriate advice from an Occupational therapist experienced with treating these situations and possibly helped by psychological interventions designed to reduce the experience of threat and encounter rational thinking. As she is over the border I cannot access the service of the Poole brain injury service but have taken the liberty of referring her to Headway Dorset who do not have this limitation and have experience in this area.”
83.	In addition, third, Mr Lillington says that his wife has undergone a profound change in her personality, emotions and behaviour:
“She gets upset by anything that she perceives to go wrong.  Situations which previously would not have bothered her, now have a bigger impact.  She becomes angry and agitated by things that previously would not have bothered her very much.” 
“Being left with a permanent brain injury has had a huge impact (on) our lives.  Sally tends to be very negative about everything and suffers from heightened emotions and feels pressurised by normal everyday tasks.  She gets very frustrated about everything and will often cry about the situation.  We do not get on well anymore.  We just co-exist in the same house.  We do not share a bedroom or spend much time together at all.” (paragraph 43 of his statement dated 23 February 2015).
That evidence is reflected in both the evidence of the Claimant herself, and in the medical records referred to above.
Breach of Duty: Relevant Findings of Fact
Introduction
84.	As I have described, although it is not contended that either Defendant ought to have foreseen that the Claimant would drink so much that she would suffer from hyponatraemia and its sequelae, Mr Spencer submitted that, at the time of the Claimant’s consultations with each Defendant on 1 October 2009, her condition of frequent and persistent vomiting was such that the Defendant ought to have admitted her to hospital, either immediately or, at the latest, within about two hours of the consultation if antiemetic therapy given at the consultation had not stopped the vomiting.  Each was negligent in not having admitted her.  Admission to hospital would inevitably have led to a blood sample being taken and analysed promptly, which would have revealed the low sodium level which would have been rectified before any seizure, encephalopathy or brain damage had occurred.
85.	Before dealing with that issue, there are various factual issues with which I must deal, particularly:
i)	the frequency, duration, pattern and nature of the Claimant’s vomiting, including (a) her presentation to the Defendants so far as her vomiting was concerned, and (b) the antiemetic medication she took, including any she took when Dr Ansell was present; and
ii)	 the severity, duration and pattern of the Claimant’s headache, including her presentation to the Defendants so far as her headache was concerned.
86.	In considering these issues, Mr Spencer criticised the record keeping of both Dr Ansell and Dr Jennison.  In particular, in the notes of their respective consultations, neither recorded the frequency of the Claimant’s vomiting or anything about headache.  Both doctors accepted that, at best, their notes were not optimal.  In cross-examination, Dr Ansell frankly described his own notes as “sloppy”, and inadequate in the ways Dr Rogers had described, i.e. in not recording the frequency, duration and amount of vomiting, any details of headache and the symptoms of cystitis from which the Claimant complained (see paragraph 1 of the joint statement dated 8 March 2015).  Dr Pambakian accepted in cross-examination that the notes ought to have included frequency and duration of vomiting. 
87.	Even allowing for the exigencies of general medical practice, I agree with Mr Spencer’s submission that the notes were, in these matters, inadequate.  Given that the Claimant’s diagnosis and the cause of the Claimant’s continuing sickness were unknown, the nature of her vomiting and any associated headache was of clinical importance; and it was important that these details were recorded for the benefit of doctors who may have been involved in the case at a later stage.
88.	However, I do not agree with his wider submission that Dr Ansell and Dr Jennison’s evidence as a whole lacks any credibility.  That submission was based, in part, upon their failure to make adequate notes; but supplemented by the following.
89.	In respect of Dr Ansell, he submitted that:
i)	There is a material discrepancy between the evidence of Dr Ansell (who says he gave the Claimant a Buccastem pill, and told Dr Jennison that he had done so), and Dr Jennison (who says he understood that the Claimant had had no such medication before he saw him later that day).  For the reasons I give below (see paragraphs 93-96), I consider Dr Ansell is wrong in this part of his evidence; and I accept that it is an important detail.
ii)	It was implausible that the doctor could recall now that the Claimant told him that she had improved and had only been sick twice that morning, when that does not appear in either the medical notes or his statement.  I accept that this part of Dr Ansell’s evidence was unsatisfactory; although I do not consider that it significantly undermines his evidence as to the Claimant’s general presentations when he saw her.
iii)	Dr Ansell gave an account to Dr Pambakian that, when he arrived at her house, the Claimant was not only up and dressed, but reading a book, which is not mentioned in the pleadings or statement.  I accept that the reference to reading a book is something of a mystery – it appears probably to have been included in some earlier notes to which Dr Pambakian had access – but in any event I do not consider it is of any great moment.  The primary point is that Dr Ansell found the Claimant up and dressed, and in a better medical condition than he had been led to expect.  Whether she had or had not been reading prior to his arrival is material, but not of any great weight.   
iv)	Dr Ansell’s assertion that he was with the Claimant for 45 minutes from noon must be regarded with caution because the Claimant made a telephone call (to her alternative medical centre in Winchester at 12.25, which must have been after Dr Ansell had left).  I agree that it is likely that Dr Ansell had left the Claimant shortly before 1225, and was therefore with her about 25 minutes and not longer (see paragraph 29 above).  Dr Ansell had calculated these times backwards from 13.00 by when he must have been back at the surgery to send off the MSU sample for analysis.  In the event, that calculation was wrong; but I do not consider that significantly affects the credibility or reliability of his other more general evidence.   
v)	There were other details of Dr Ansell’s evidence that were not reliable.  For example, first, Dr Ansell said that he recalled discussing echinacea with the Claimant, who told him that she had taken the product throughout her illness.  The Claimant denies this, because she has never had echinacea in her house, and has never taken it.  The evidence with regard to echinacea (or “econashia” in the medical records: see paragraph 21 above) is certainly mysterious.  How that reference came to be in the records, if the Claimant never mentioned it to Dr Shaw, is certainly odd.  However, it is of no substantive moment; because it has never been suggested that any ingestion of echinacea caused the Claimant any symptoms, and she never suggested to any healthcare professional that it had.  It is a matter that only goes to Dr Ansell’s credibility.  I shall, in favour of the Claimant, proceed on the basis that Dr Ansell’s recollection of that part of the conversation was incorrect.
vi)	Second, Dr Ansell gave evidence that he gave the Claimant dehydration advice when he saw her on 1 October (see paragraph 32 above).  In paragraph 27 of his statement of 7 October 2014, he said:
“I said that while such fluids could include water, a better alternative would be Dioralyte, or an alternative commercial equivalent electrolyte powder made up with water as a drink; such preparations were available from any chemist.  She could also use diluted fruit juice or squash with a pinch of salt.  I always recommend one teaspoon of salt with one and half pints of liquid.  I also mentioned the alternatives of tea without milk, many adults drink a lot of tea.  I do recall discussing these options with her.  She appeared to understand the advice that I was giving to her, and seemed prepared to follow it.”
Both the Claimant and Mr Lillington denied that such advice was given: had it been, they said, they would have followed it.  the Claimant said that she knew that Dioralyte was not a drug as such, and she had taken it before (as her medical records confirm).  She would have had no aversion to taking it then.  However, I am persuaded that Dr Ansell did give this advice to the Claimant.  It is noteworthy that Dr Denman is recorded as having given the Claimant “gen adv re hydration”.  Mr Lillington said that his wife did not tell him that she had been advised to take antiemetic medication – and, indeed, had been prescribed it.  Although the Claimant said she would have regarded Dioralyte in a different light from Buccastem, I consider it is likely that she was given advice concerning Dioralyte by Dr Ansell, but neither acted upon it nor did she disclose that advice to her husband.
90.	In relation to some of the details of his evidence, I accept that Dr Ansell was far from a satisfactory witness.  He himself accepted that he did not recall all of the details of the consultation; but, he said, he did recall the “principles”.  I accept that: whilst I found some of the details of his evidence – including, I must say, some important details – to be unreliable, in my judgment that was a result of an honest, but faulty, attempt to recollect what happened at the relevant time.  Unfortunately, in my view, genuine attempts at recollection became unconscious reconstruction.  However, having seen Dr Ansell give his evidence, I do not consider that those failures with regard to detail significantly undermines his evidence with regard to general matters; and, specifically, I accept his evidence as to the general presentation of the Claimant, to which I shall come shortly.
91.	In respect of Dr Jennison, Mr Spencer submitted that:
i)	Dr Jennison’s evidence that he asked the Claimant about headache, and she denied having (or having had) a headache.  That, Mr Spencer submitted, is incredible, if, as the firm evidence suggests, she had had the “worst headache ever” only the day before.  
ii)	Dr Jennison’s evidence about what the Claimant’s history of vomiting was unsatisfactory.  The doctor said that he asked about the frequency of vomiting, but (a) did not record any response, and (b) cannot now recall the Claimant’s response – except, he said, she said that she had vomited since seeing Dr Ansell; and, if he had been told that she had been sick every 20-30 minutes for three days, he would have recorded that, because it would have been such a remarkable history.    
92.	I again agree with Mr Spencer that the inadequacy of the notes is unfortunate, and Dr Jennison’s evidence in relation to both headache and vomiting was not altogether satisfactory.  In particular, although by the time the Claimant saw Dr Jennison I am satisfied that her headache had resolved (and the Claimant herself appears to have attached little importance to it), I am unconvinced that the Claimant denied she had had a headache during any part of her illness, after direct questioning by Dr Jennison, as he recollects.  I do accept that she led him to believe that she did not have a headache at the time of the consultation, which was indeed the case.  
93.	However, again, on all of the evidence, I am satisfied that, despite these deficiencies as to detail, Dr Jennison’s evidence as to the Claimant’s general presentation when he saw her was reliable.  He said that she presented with nausea, not vomiting, and was not as poorly as he had been led to believe she might have been.  I do not accept Mr Spencer’s submission that it is implausible that the Claimant was better than she had been, but nevertheless approached the surgery that evening and then saw Dr Jennison.  As Dr Jennison said, she was still “not right”; and, although her vomiting may have been better than it had been, by 18.30, it is likely that the symptoms of nausea deriving from hyponatraemia were kicking in.  On any view, she was still poorly.    
Dr Ansell and Buccastem
94.	There is a discrete issue as to whether Dr Ansell gave the Claimant the antiemetic pill, Buccastem, i.e. as well as giving her a second pill for later, actually saw her ingest a pill whilst he was with her.
95.	In his oral evidence, Dr Ansell said that, during his consultation with the Claimant, she confirmed that, although having been prescribed antiemetic pills by Dr Shaw on 29 September (and advised by Dr Worden on 30 September to take them, if her sickness persisted), she had not taken any antiemetic medication.  He said he recalled giving her two Buccastem pills, one of which she took whilst he was there, and the other she saved for use later if required.
96.	However, I am unable to accept that evidence.
i)	Dr Ansell made no note of having given the Claimant that medication.  Mr Spencer submitted, with some force, that, if Dr Ansell had administered that drug, he would have made a note of it.  
ii)	Dr Ansell accepted in cross-examination it was clinically “extremely important” that he had given her an antiemetic because, if her vomiting continued, it would be continuing despite that treatment.  
iii)	Dr Ansell accepted that it was also important that Dr Jennison (or any other doctor following up Dr Ansell’s consultation later) knew that that medication had been given.  Dr Ansell said that he thought he recollected telling Dr Jennison that he had given the Claimant Buccastem when he spoke to him on the telephone that afternoon; but (a) Dr Jennison could not recall being told that by him, and (b) even more potently, Dr Jennison said that the Claimant gave him to understand that she had not had any antiemetic treatment.  He could not sensibly have had that understanding if Dr Ansell had told him he had given Buccastem to the Claimant.
iv)	There is no reference to Dr Ansell giving the Claimant an antiemetic pill in (a) Dr Ansell’s letter of response to the pre-action protocol letter, (b) Dr Ansell’s Defence, or in any of its amended forms, (c) Dr Jennison’s statement or (d) in the reportage given to Dr Pambakian by Dr Ansell.  Indeed, that reportage appears to have been to the effect that such medication was advised, but not given (see paragraph 8.17.4, 8.17.5 and 8.19.3 of Dr Pambakian’s report dated 28 November 2014). 
v)	The Claimant was averse to having oral antiemetic medication when she saw Dr Jennison later that day, preferring to have an injection         
97.	Therefore, I consider Dr Ansell’s recollection in this regard is wrong.  I find that, although he gave the Claimant two Buccastem pills, he did not supervise her taking one of them; nor did she in fact take one.  Later that day, she rightly led Dr Jennison to believe that she had not taken any antiemetic medication before the consultation with him.
The Claimant’s Vomiting etc
98.	Generally with regard to the nature and pattern of the Claimant’s vomiting, Mr Spencer submitted that I should find reliable the evidence of Mr Lillington, supported by the medical records, to the effect that the Claimant vomited continuously and without improvement, every 20-30 minutes, from within minutes of taking the antibiotic pill early morning on 29 September to her collapse in the early hours of 2 October 2009; and I could, with confidence, make a finding to that effect.  
99.	There are, of course, difficulties with the evidence relating to the Claimant’s vomiting.  The Claimant herself suffers from amnesia, and cannot recall anything from that period.  Mr Lillington was at work during each day.  Although he was at home during the early mornings, evenings and over night, the Claimant made it clear that she wished to be on her own, which he respected.  Therefore, although he heard her being ill, he did not see the Claimant vomit to any great extent.  Furthermore, neither Dr Ansell nor Dr Jennison recorded the frequency of vomiting in the medical records.  The evidence is therefore generally sparse on this issue.
100.	However, we do have a transcript of the Claimant’s conversations with the out-of-hours service, during the night of 1-2 October 2009, shortly before her collapse.  Mr Spencer suggested that the conversations might not convey the true picture – but, despite her obvious distress at the time and her subsequent amnesia, there seems to me to be no reason to suppose that the Claimant’s presentation and description of symptoms was underreported or otherwise inaccurate.  I appreciate that the Claimant was ill and the subject of some distress at the relevant time, but she herself said in evidence that, had she been vomiting frequently, she thought she would have made that clear to those to whom she spoke. 
101.	The focus of the conversations was upon the Claimant’s symptoms, which she described, not in terms of being sick or vomiting every 20-30 minutes, but of feeling sick.  Of course, “nausea” and “vomiting” are often used loosely.  It is possible to dry retch without producing any vomit.  Furthermore, when a patient is in distress, he or she can be forgiven for not using words and phrases with exactitude.  But, here, the Claimant initially complained to the triage nurse that, although she had been vomiting for three days, she had had an antiemetic injection at 18.30 and “now feeling nausea”.  The symptoms are described in terms of “feels very sick”, and the presenting complaint as “nausea”.  Over the telephone that evening, the Claimant did not present with continuous vomiting: rather, she consistently complained of “feeling sick” or even “feeling she was going to be sick”; and, upon questioning, agreed that she had actually been sick “just the once” about 2-3 hours before the phone call after 2am (i.e. about, say, midnight).  Mr Spencer submitted that this was, or might be, limited to a reference to vomiting with blood – but, when seen in the context of the conversations as a whole, it was clearly a reference to vomiting at all.  When it was put to her on the telephone, she agreed that it was “the feeling of nausea” that was the problem; and said, “I’ve never had feeling sick like it”.  
102.	Although Mr Lillington recalls something different and Dr Bajaj recorded in his initial interview with the Claimant, “Pt has been vomiting for 3 days”, the picture painted by the Claimant herself that evening is clear: she had been vomiting regularly but, since the antiemetic injection at 18.30 that evening, the pattern of her vomiting had stopped – she had vomited only once – but she had been feeling very poorly, and increasingly poorly, with nausea.  It is noteworthy that there is no evidence of the Claimant vomiting during Dr Bajaj’s visits, or in the ambulance, or once she had been admitted to hospital.   
103.	The experts provided a likely explanation for this.  The cause of the Claimant’s original vomiting has never been determined.  It may have been an adverse effect of taking nitrofurantoin: both Dr Ansell and Dr Jennison agreed that nausea and vomiting are a recognised side effect of that drug.  It certainly was not caused by hyponatraemia, because there is no evidence that the Claimant had been drinking excessively before she started to vomit and in any event the experts are agreed that any symptoms from that condition were not likely before the morning of 1 October 2009.
104.	However, nausea and vomiting are also recognised symptoms of hyponatraemia.  Dr Almond said that hyponatraemia is usually asymptomatic unless severe; but, once the sodium serum level is below 125 mmol/L, “you can expect to see some symptoms amongst which nausea and vomiting may occur”.  He calculated, on a straight-line basis, that the Claimant’s level would have fallen to 125 mmol/L by perhaps 4am on 1 October 2009.  There are many variables and many reasons why the decline might not have been straight-line – indeed, there is evidence that the Claimant’s decline during the evening of 1 October was rapid.  However, Dr Ahlquist accepted that as a reasonable rough estimate; and, in any event, he agreed that there came a point from when it is reasonable to attribute the nausea or vomiting suffered by the Claimant (or, at least, some of it) to her hyponatraemia.  I accept that.          
105.	In my view, the evidence points towards the following.  
106.	The symptoms of the Claimant’s vomiting had lessened by the time she saw Dr Jennison; and were further alleviated by the antiemetic injection administered by him at about 18.30 on 1 October 2009.  Mr Lillington recalled, in (I accept) firm and clear terms, how his wife vomited within minutes of returning from the surgery visit to Dr Jennison, and regularly thereafter at intervals of 20-30 minutes or so.  However, I am unable to accept that evidence.  Mr Lillington was no doubt distressed by the events of that evening; and, in my view, his recollection as to this is, unfortunately, mistaken.  The evidence overall – and, particularly, the evidence of the Claimant’s telephone calls with the out-of-hours service that night – points firmly to the injection being effective, and the Claimant vomiting only once after that injection, at about midnight.
107.	The Claimant did, however, continue to feel very poorly following her return from seeing Dr Jennison.  In her series of increasingly distraught telephone calls from about 21.20 onwards, she complained to the out-of-hours service as to how nauseous she felt.  The feeling of nausea worsened as the evening wore on.  Mr Lillington described how she went “rapidly downhill” that night.  Dr Howard considered that the Claimant’s sodium levels may have dropped precipitously in the few hours before her fits, once her normal renal mechanisms for maintaining sodium levels had been overloaded (paragraph 3 of the joint statement dated 4 October 2015); and Drs Almond and Ahlquist agreed that there may have been such a drop and, whatever the precise line of descent, “it is very likely that there was a further significant decline in the level of serum sodium in the final 12 hours prior to the onset of [her] seizures” (paragraphs 18-19 of their joint statement dated 12 October 2015).  It is noteworthy that, once the Claimant’s sodium levels started to be restored in hospital, she was not sick again, nor is there any record of her felling nauseous.  On the balance of probabilities, by the evening of 1 October 2009, the symptoms of nausea suffered by the Claimant did not derive from the cause of the original sickness, but wholly or predominantly from her hyponatraemia.        
108.	Consequently, I do not consider that the Claimant did vomit as claimed, after her visit to Dr Jennison at 18.30 on 1 October 2009.  
109.	Indeed, although I accept that she was ill, and vomited from time-to-time during the period from shortly after she took the antibiotic pill on the morning of 29 September until she saw Dr Jennison, I do not accept that she vomited every 20-30 minutes (or anything like that frequency) throughout that period.  In coming to that conclusion, I have particularly taken into account the following.
i)	There is, of course, no evidence from the Claimant to that effect.  
ii)	The evidence was that, generally, the Claimant would not take medicines unless she needed to: for example, she said that she would only take painkillers if necessary.  The Claimant was prescribed Buccastem for her sickness on 29 September, and advised to take it the next day if her sickness required it; but she did not take any medication for her vomiting.  I understand that she night have been reluctant to take any further medication, as she thought her condition had been triggered by taking nitrofurantoin earlier.  Nevertheless, her failure to take prescribed medicine as repeatedly advise suggests that her vomiting was not as serious, frequent or debilitating as now suggested.
iii)	Mr Lillington did describe seeing his wife being physically sick – but only on a couple of occasions.  He was not at home during the day on any of the three days in question, and, when he was at home, he kept his distance, the Claimant understandably wishing to have her privacy.  Whilst he says that the house being small and the walls thin, so he could hear his wife being ill –– he accepted that he slept during each night, if fitfully, and the sounds he heard could have been the Claimant retching rather than vomiting.  Indeed, during cross-examination he appeared to accept that, at night, he heard his wife retch, and did not know whether she was physically vomiting or not.
iv)	The evidence was of Mr Lillington being a caring husband.  However, he did not stay at home during this period of his wife being ill.  He was at work during the day.  He slept in the spare room at night.  He did not, e.g., seek medical assistance for her.  He considered that it was under control.  When he went to the doctor’s surgery with the Claimant to see Dr Jennison on the evening of 1 October, he did not go into the surgery with her.  His actions were not consistent with his wife being physically sick every 20-30 minutes over a three day period.
v)	Drs Almond and Ahlquist agreed that vomiting continuously for three days would likely lead to dehydration, and the Claimant in fact had water overload.  They consider that she may have had dry retching in addition to vomiting in the period from 29 September 2009 (paragraph 17 of their joint statement dated 12 October 2015).
vi)	I am unable to accept all of the evidence of Drs Ansell and Jennison; and I deal with relevant elements of their evidence which  I do not accept elsewhere in this judgment.  However, both said that, on their respective consultations on 1 October 2009, the Claimant did not present as someone who had been vomiting to the extent that is now suggested; and, whilst (as I have indicated) I cannot accept all of the detailed evidence they gave, I do accept the evidence of the two doctors as to her general presentation when they saw her.  Indeed, it seems to me that the fact she did not appear to be as ill as they had expected – coupled with the examination conducted by each, which reasonably ruled out serious pathologies – probably led them to be less than optimal in their note-taking.  Having seen the doctors give evidence, I am satisfied that, had the Claimant presented as being exhausted with the physical effort of continuous vomiting over several days, they would have recalled that – and, indeed, made reference to it in the notes that they did make.  The Claimant did not present to either as someone who had been continuously vomiting over 2-3 days.  She was not sick during either of those consultations.  I have already dealt with their record keeping deficiencies (see paragraphs 86 and following above); but the Claimant did not report to either that she was vomiting as frequently as now claimed.  Dr Ansell described how she was up and dressed, when he attended her at home at about noon that day; and there were no signs of recent vomiting.  She did not appear to be distressed.  She told Dr Ansell that she had been sick frequently over the last two days, but it was less severe that morning when she had only been sick twice over a period of about three hours.  To Dr Jennison, she did not seem to be particularly unwell, although she appeared to be anxious.  She presented primarily with nausea, rather than vomiting; although she did not appear to the doctor to be unduly nauseous either.  She did not carry a bowl with her into the consultations with him.
vii)	It is noteworthy that the Claimant did not report being sick to the out-of-hours service on the evening of 1-2 October 2009; and she was not physically sick during the home visit of Dr Bajaj.  
110.	Therefore, although I accept that the Claimant was poorly from the morning of 29 September until she collapsed early in the morning of 2 October 2009, I am not persuaded that she was vomiting every 20-30 minutes throughout that period.  Indeed, by the time she saw Dr Jennison her vomiting was, at worst, less than it had been; although, by then, she was suffering from nausea as a symptom of hyponatraemia.
The Claimant’s Headache
111.	The evidence as to the Claimant’s headache was more straightforward.
112.	Mr Lillington said that the Claimant complained to him of a severe headache on the morning of the second day of her illness, 30 September.  She told him, that evening, that she had got the worst headache she had ever had; but she did not tell him anything about the speed of its onset.  She did not complain to him of a headache on 29 September; and Mr Lillington accepted that he must have been the source of the reference in Dr Stallard’s letter dated 16 October 2009 to the effect that he understood that the headache disappeared on 1 October but she suffered further headache just before her seizure.   
113.	That lay evidence is reflected, to an extent, in the medical records.  When the Claimant spoke to Dr Denman at 13.30 on 30 September, the doctor recorded:
“Nitrofurantoin caused sickness and headache” (emphasis added).
Dr Worden did not record headache in the notes when she spoke to the Claimant later that day.
114.	As I have described, neither Dr Ansell nor Dr Jennison made any note with regard to headache.  
115.	Dr Ansell said in his evidence that the Claimant had not spontaneously referred to headache when he saw her; but, on being questioned, she said that she had had a headache which began after the vomiting had started, and which she still had that day.  It was mild, but had been worse the day before.  She described it (he said) as mild but persistent.  
116.	Dr Jennison said that he asked the Claimant whether she had (or had had) a headache, and she said she had not.  As I have already indicated (paragraph 92 above), I do not accept that the Claimant told Dr Jennison that she had never had a headache during her illness, as he recalls; although I do accept that she probably told him that she did not then have a headache.  The fact that she did not tell Dr Bajaj – as well as Dr Jennison – about it, indicates that, despite its actual clinical significance, the Claimant herself did not regard it as of any particular importance.
117.	When Dr Bajaj attended the Claimant for the first time, neither he nor the Claimant referred to a headache.  By the time of his second visit, a subarachnoid haemorrhage was suspected, and that suspicion affected the recorded notes.  “Sudden onset” and “thunderclap” headaches – characteristic of subarachnoid haemorrhage – are recorded, but there is no contemporaneous evidence of the Claimant having suffered such a headache.  As I have indicated (see paragraph 57 above), the only source of such a report was Mr Lillington; and he was never told by his wife that the onset of her headache was sudden (or, indeed, that it had lasted for five days, as some of the records suggest).
118.	The evidence with regard to the headache the Claimant suffered is therefore reasonably firm.  She suffered a bad headache on 30 September, which she reported to Dr Denman.  The Claimant neither took nor sought any medication for it.   The headache had waned by 1 October.  By the time she saw Dr Jennison it had resolved.  The record of the headache after the Claimant had fitted derives from Mr Lillington, as interpreted by the healthcare professionals in the light of the suspicion that the Claimant had suffered a subarachnoid haemorrhage.  It does not accurately reflect the headache the Claimant had in fact suffered.  However, the Claimant suffered second headache shortly before she had her first seizure.  Headache is, of course, a symptom of hyponatraemia.  This further headache appears to have been relatively mild, because it was not reported to the out-of-hours service or Dr Bajaj or by Mr Lillington immediately following the seizures.  
The Law
119.	The test to be applied for assessing whether the conduct of a healthcare professional is negligent is well-settled, and I need not dwell on it at any length.  
120.	The law recognises that, in the field of medicine, there are different schools of thought, several of which may constitute a reasonable opinion.  A doctor is not negligent is the course of treatment he undertakes is in accordance with a responsible school of thought (Bolam v Friern Hospital Management Committee [1957] 1 WLR 582 at page 587 per McNair J, subsequently affirmed and applied by the House of Lords in Whitehouse v Jordan [1981] 1 WLR 246 and Maynard v West Midlands Regional health Authority [1984] 1 WLR 634, as explained in Bolitho v City and Hackney Health Authority [1997] UKHL 46.
121.	In this case, Mr Spencer submitted – fairly – that the question in relation to breach of duty is consequently whether the Claimant is able to show that no reasonably competent general practitioner, in the circumstances in which each of Dr Ansell and Dr Jennison in fact found himself, would have acted and exercised his judgment in respect of his treatment of the Claimant in the way that Dr Ansell and Dr Jennison respectively did. 
Discussion and Conclusion
122.	Having dealt with those factual issues, I can deal with the issue of breach quite shortly.
123.	There was, essentially, not a great deal in issue between Dr Rogers and Dr Pambakian, the general practice experts who gave evidence on the issue of breach of duty.  The evidence of Dr Rogers – overall, an impressive witness – is an appropriate starting point.  
124.	Dr Rogers readily conceded that vomiting and headache are commonly encountered in general medical practice, and it is not necessary or appropriate to admit to hospital all patients suffering from one or both of these conditions.  He confirmed that which we know from our own experience: many patients simply recover from vomiting without medication.  For most others, he said vomiting will normally respond to an antiemetic, which will usually offer symptomatic relief. 
125.	However, Dr Rogers said that there were two reasons why vomiting of some considerable frequency and/or duration might be a cause of concern, and warrant hospitalisation.  First, it can be associated with some other, serious condition which might not be capable of diagnostic exclusion without the benefits of hospital facilities.  Second, vomiting in itself can be serious, and even life-threatening: a person suffering from persistent vomiting will lose fluid and stomach acid, and may become physically exhausted by the extended trauma of being sick.  
126.	In this case, Dr Rogers accepted that both Dr Ansell and Dr Jennison conducted an examination of the Claimant properly to exclude serious illnesses (such as diabetes, subarachnoid haemorrhage and meningitis) from diagnosis.  Indeed, Dr Rogers considered Dr Jennison’s assessment of the Claimant to exclude serious pathologies as “commendable”; and he made no criticism of it.  
127.	Continuing to focus upon Dr Jennison for the moment, on the basis that (as I have found) the Claimant had not had any antiemetic treatment prior to seeing Dr Jennison, nor did Dr Rogers criticise Dr Jennison for giving the Claimant an intravenous antiemetic to see whether it would stop her vomiting.  In his view, as I understood it, many doctors would have admitted the Claimant in the circumstances in which Dr Jennison saw her in the early evening on 1 October 2009.  Indeed, it seems that Dr Rogers may fallen firmly into that camp.  However, he readily accepted that (in his words) “a reasonable, if minority, body of general practitioners” would consider it appropriate to have given an intravenous antiemetic in those circumstances; and, they would not have considered a hospital admission called for, if that had “stopped” the vomiting.  Dr Rogers considered that, for that course to be appropriate, the doctor would have had to have made clear to the patient that, if the vomiting did not stop immediately, then the patient should go to hospital.  However, he accepted that, if the patient had generally stopped vomiting, and then vomited (say) just once some hours later, then it would have been considered appropriate advice to have required the patient then, not to attend hospital straightway, but to seek further advice by telephone.   
128.	Therefore, Dr Rogers did not consider the safety netting advice which Dr Jennison gave to the Claimant – i.e. if she worsened or had any concerns overnight, she should call the out-of-hours service or go to A&E at the hospital – to have been sufficiently specific or firm.
129.	However, as I have found, the antiemetic injection did “work” in the sense described by Dr Rogers: it broke the pattern of vomiting from which the Claimant had suffered, and she was sick only once more, at about midnight.  She had, before she had vomited again, contacted the out-of-hours service, and a doctor was on the way.  
130.	Dr Pambakian considered the standard set by Dr Rogers to be too high, in the sense that he considered that it would be reasonable not to send a patient to hospital in circumstances in which Dr Rogers considered such a course mandated.   Given the presentation of the Claimant when she saw Dr Jennison, I am persuaded that the safety netting advice he gave to her was appropriate.
131.	However, even if I am wrong in that regard, even if Dr Jennison had given the Claimant precisely the advice that Dr Rogers considered appropriate, then the course of events would not have changed.  In following that advice, the Claimant would have contacted the out-of-hours service for further advice when she did, or at least no later than about midnight when she was sick again.  That service gave her advice, about which no complaint is made.  In the circumstances, on any view, in my judgment Dr Jennison was not arguably in breach of duty.  
132.	Nor was Dr Ansell.  Dr Rogers again accepted that Dr Ansell conducted an examination of the Claimant properly to exclude serious illnesses from diagnosis.  Whilst Dr Rogers did not accept that, in the circumstances in which Dr Ansell found himself, it would have been appropriate for him merely to advise, even if strongly, the use of an oral antiemetic:
i)	Given the Claimant’s presentation to Dr Ansell as I have found it to have been, I would conclude that a recommendation to use such medication would have been appropriate, if (as I have found) the doctor considers that the patient will follow that advice.
ii)	In any event, Dr Ansell gave appropriate advice to the Claimant to contact Dr Jennison if she was no better; which she did.
iii)	In the particular circumstances of this case, as Dr Jennison was not negligent, it is difficult to see how any breach of duty by Dr Ansell could have been material.   
Conclusion
133.	For those reasons, I conclude – firmly – that neither Dr Ansell nor Dr Jennison breached his duty of care towards the Claimant.  That is sufficient to dispose of this claim, by dismissing it.  
134.	However, I heard substantial submissions on two other issues – legal causation and medical causation – and, out of deference to those submissions, I should deal with them, if somewhat more briefly than if they had been determinative of the claim.
Legal Causation
135.	I have set out the issue, briefly, above (see paragraph 5 (ii)).  
136.	The Claimant had severe acute hyponatraemia as a result of psychogenic polydipsia, which caused her seizures, encephalopathy and (it is said) some degree of brain damage.  Drs Rogers and Pambakian agreed that it was not reasonably foreseeable that the Claimant would drink excessive amounts of water, or would suffer from hyponatraemia (paragraph 32 of their joint statement dated 8 March 2015).  It was also common ground that, as at 19.30 on 1 October, the Claimant’s serum sodium level would have been significantly greater than 105 mmol/L. and above the level that seizures were likely to occur.  If and when the Claimant had been referred to hospital on 1 or 2 October 2009, her management would have been materially similar to that she in fact received when she was admitted in the early hours of 2 October.  In particular, she would have been the subject of the same blood tests, with the same immediacy.  Thus, had she been referred by (say) 21.00 on 1 October following the intervention of Dr Jennison (which, on this hypothesis, would have been “unsuccessful” in the terms of Dr Rogers’ analysis), her hyponatraemia would have been detected and treated before she suffered any encephalopathy or further damage to her brain.  She would quickly have returned to the condition she had been in before these events, as described above (see paragraphs 17-18).
137.	Given that Mr Spencer concedes that the condition from which the Claimant in fact suffered as a result of any negligence of the Defendants – hyponatraemia and consequential encephalopathy etc – was not foreseeable, legal causation is not straightforward.  
138.	However, Mr Spencer submitted that this scenario fell within the scope of Hughes v The Lord Advocate [1963] AC 837, in which an 8-year-old boy suffered very severe burns after entering a workman’s tent in the street and knocking over a paraffin lamp into a hole causing an explosion.  It was held by the House of Lords that the workmen were negligent in leaving the lamp as they had done; and they were liable to the boy for his injuries because the lamp was a foreseeable source of danger and burns were a foreseeable type of injury, although in the event that source of danger acted in an unpredictable way and the burns were of a different degree to those that were foreseeable.
139.	 Mr Spencer submitted that, in the Claimant’s case, the damage that occurred – seizures, encephalopathy and any damage to the brain that resulted – were “within the risk created by the negligence” of the Defendant doctors.  
140.	His narrow ground was based upon the expert evidence that, certainly by the time Dr Jennison saw the Claimant, her symptoms of vomiting and/or nausea were caused by her hyponatraemia.  
141.	His wider ground was bolder.  He submitted that, by failing to refer the Claimant to hospital when they ought to have done, the doctors created a risk that a condition which would have been detected, would go untreated with serious adverse consequences for the Claimant.  In that regard, it did not matter that the doctors could not have been expected to foresee that the Claimant would suffer from hyponatraemia, caused by psychogenic polydipsia or otherwise.  It is enough that it could reasonably have been foreseen that, if the Claimant was not referred to hospital, she might come to harm from some medical condition that was not reasonably foreseeable, which they (the doctors) were not in a position to diagnose but which a hospital would diagnose with the availability of its greater investigatory facilities.  This is consistent (Mr Spencer submitted) with the gate-keeping function of a general practitioner, whose duty it is to recognise when a patient needs to be sent to hospital for further investigation.
142.	Mr Porter, on the other hand, submitted that the risk of hyponatraemia did not fall the Hughes formulation of “within the risk created by the negligence”, liability for negligence being limited to the consequences of what made the acts wrongful.  It was not sufficient for the legal causation that some injury was reasonably foreseeable, and some (other) injury was sustained.  Rather, this case is akin to the well-known mountaineering example used by Lord Hoffmann in South Australia Asset Management Corporation v York Montague [1997] AC 191 at page 213: a doctor who advises a mountaineer wrongly and carelessly about his knee is not liable to that mountaineer if he sustains injury in an avalanche, because the damage suffered is too remote as a matter of law.  In this case (Mr Porter submitted) neither doctor would have been liable for injuries the Claimant might have suffered if there had been a fire at her home at a time when (but for their negligence) she would not have been at home but in hospital.  Any injury she suffered as a result of hyponatraemia falls within the same category.
143.	A submission based upon “piggy-back” causation is never easy.  The jurisprudence, in the field of medical negligence, is sparse: despite their diligent researches, Counsel were unable to identify any cases on point from that field.  
144.	Given that this issue is not determinative in this case, it is unnecessary for me to arrive at a firm conclusion; and I decline to do so.  However, my provisional view is that this claim would not have foundered on legal causation.  As Mr Spencer submitted, even if the reliability of the straight-line approach adopted by Dr Almond (see paragraph 104 above) may be the subject of debate, and even doubt, the evidence of the expert physicians was that the symptoms of nausea with which the Claimant was presenting when Dr Jennison (and, quite possibly, Dr Ansell) saw the Claimant were or included symptoms of hyponatraemia.  Dr Rogers asserted that the Claimant ought to have been referred to hospital as a result of her persistent vomiting.  Nausea and vomiting are different conditions: but, it seems to me, it is at least strongly arguable that they are a similar type of injury – and, thus, the Defendants might have had real difficulties in escaping liability on the basis that the damage suffered was different in kind from the damage that was reasonably foreseeable.  Indeed, in this case, Mr Spencer’s wider ground also appears to me to have some force  
145.	Consequently, I am provisionally persuaded by Mr Spencer’s submissions in relation to legal causation.
Medical Causation
146.	If legal causation in this case is not straightforward, medical causation is particularly challenging.
147.	Mr Spencer submitted, with force, that there has been a significant and permanent change in the Claimant’s condition, behaviour and physical and mental health since her episode of hyponatraemia and its immediate consequences.  I accept that the changes have been, if not permanent, certainly long-term: she is still suffering from them, some five and a half years after the event.  I also accept that these changes are not only since, but as a result of, that episode.
148.	As Mr Spencer submitted, amongst the prolific amounts of expert evidence, two explanations are proferred: organic brain injury with (in psychiatric terms) a resultant Frontal Lobe Syndrome (“FLS”) falling within Class F07 of the Tenth Revision (2010 Edition) of the WHO International Statistical Classification of Diseases and Related Health Problems (“ICD 10”), namely Personality and Behavioural Disorders due to Brain Disease, Damage and Dysfunction; or there is a purely psychiatric condition without any organic foundation which would be or have been classified as a somatoform disorder, a somatic symptom disorder, a conversion disorder, hysteria or a functional neurological disorder.  The key distinguishing factor between those two options is, of course, that the former is based upon organic brain injury and the latter is not.   
149.	The Claimant’s case, from the outset, has been based upon the premise that her injury is an organic brain injury.  That has been an essential element in her case.  That is how it was pleaded in paragraph 39(9) of the original Particulars of Claim and in all subsequent pleading iterations, and that is how Mr Spencer opened the case.  It is also the basis upon which all the expert evidence was prepared and presented.  
150.	In his closing submissions, Mr Spencer applied, informally, to amend the claim to include an alternative claim based, not upon an organic brain injury, but upon the Claimant’s “psychological reaction to [her hyponatraemia and encephalopathy]”.  Mr Porter opposed such amendment, in part on the basis that the Defendants had prepared on the basis of the pleaded case and, if they had a new case to meet, they may have prepared differently and would certainly now wish to consider and respond to the new case.  I agree.  It is simply too late to allow such an amendment.  The Defendants would clearly have approached this case differently had they been facing this additional, alternative claim.  The Claimant has always firmly fixed her colours to the mast of organic brain injury: and, if causation were determinative, she would properly be restricted to that case.  I formally refuse that application.
151.	However, medical causation remains a difficult issue.  As we shall see, each possible diagnosis has serious difficulties with which to contend.  
152.	Although, in his oral evidence, Dr Leng said that he considered the neuropsychological testing results he obtained from the Claimant were diagnostic of organic brain damage and FLS (thus diagnostically excluding a non-organic pathology):
i)	Conventionally, psychologists do not diagnose: they provide evidence upon which others can base a diagnosis.
ii)	That view goes contrary to paragraph 29 of the joint statement of experts dated 15-16 October 2015, in which Dr Leng agreed that his report was merely “consistent with [FLS]”, and not diagnostic of it.  Where there are only two potential diagnoses, for results to be merely consistent with one, necessarily implies that they are also consistent with the other.  In the same joint report (at paragraph 33), the expert psychiatrists (Drs Shotbolt and Isaac) agreed that the reported symptoms and their clinical findings were consistent with both FLS involving organic brain damage and “mood disturbance and anxiety”.
iii)	For the reasons given below (see paragraph 157), the results of neuropsychological testing do not appear to be as compelling as Dr Leng suggested in his oral evidence.
153.	Otherwise, all of the experts agreed that the evidence was consistent with both FLS involving organic brain damage and a psychiatric condition that did not – none suggested the evidence precluded either – although, of course,  each considered that the evidence favoured one or the other.
154.	The main strands of evidence that supported the proposition maintained by Mr Spencer, that the Claimant suffers from organic brain damage, were as follows.
i)	Some of the healthcare professionals who treated the Claimant clinically (notably Dr Stallard who refers to “neurological/brain injury” in his note of 22 October 2009, and Dr Burn) indicated, albeit far from unequivocally, that they considered that she might have suffered an organic brain injury.  However, Dr Stallard appears to have considered that hypoxia and/or demyelination may have played a part which, the experts now agree, they did not.  
ii)	During the course of the hearing, Dr Howard (the neurologist instructed by the Defendants) changed his stance on the re-admission of the Claimant to hospital on 15 October 2009, and it became common ground that the Claimant was encephalopathic for 5-6 weeks after her episode of hyponatraemia and cerebral oedema which was short (hours, and certainly no more than a couple of days).  Following such a relatively minor insult to the brain, such a period of encephalopathy without succeeding organic brain damage is unusual: indeed, even Dr Howard said that, in his experience, it would be unique.
iii)	The Claimant’s presentation is generally typical of FLS, and atypical of a somatoform disorder.  Dr Isaac (the psychiatrist instructed by the Defendants) said that he had clinical experience of one such case – where a patient without organic brain damage had presented with the FLS constellation of symptoms – but that patient was also psychotic (schizophrenic), which the Claimant clearly is not.  The evidence was that, where a condition is purely psychological in origin, it usually presents differently, e.g. by way of functional paralysis, non-epileptic seizures, functional blindness functional sensory loss, and discrete memory problems.  The Claimant notably complains of none of these.
iv)	As well as being consistent with FLS, the impairments from which the Claimant continues to suffer are consistent with the features observed during her acute illness in 2009 (see paragraph 7.8 of Professor Chadwick’s report dated November 2014).
v)	Dr Leng conducted a battery of psychological tests on the Claimant which, it is agreed, were valid. (The Defendant’s expert, Dr Bach conducted similar tests, but did not obtain valid results as a consequence of the Claimant failing properly to engage with the tests.)    Dr Leng said that these tests showed a significant impairment of executive function, wholly in keeping with FLS.  I deal with this evidence separately below (see paragraph 157).  
155.	The main evidence which supported Mr Porter’s contention – that the Claimant’s condition is not one involving organic brain damage – was as follows.
i)	All of the experts accepted that at least some of the Claimant’s current symptomatology is psychological in nature, i.e. it does not have an organic cause.  The Claimant herself accepted that he headaches and lethargy “depend on life events”.  The extracts from the post-index event medical records above (paragraphs 70 and following) show that, after her hyponatraemic episode, the Claimant continued to suffer from symptoms that were associated with specific stressors; and her main complaint is in respect of headache.  She confirmed to Dr Leng that that was the case (paragraph 3.2 of his report dated 24 July 2012).  It is common ground that the headaches from which she suffered, and continues to suffer, are not caused by organic brain damage, but are psychological in nature, probably resulting from anxiety, stress and/or depression.  Professor Chadwick accepts that these symptoms cannot be attributed to any acute encephalopathy, but result from her “anxieties” (paragraph 4.4 of his report dated February 2015).  
ii)	The Claimant had a history of psychological conditions, apparently reflecting an inability to cope well with stress.   It is important that this is kept in perspective – the Claimant had long symptom-free periods, including the period 1997-2008 – but in 1993-95, she suffered from a serious episode of CFS, which recurred in 2003 and 2006.  In the period May-July 2009, it is recorded in the medical records as being “brought… back with a vengeance”.  Indeed, when discussing her condition with the out-of-hours service in the early morning of 2 October 2009, she volunteered: “I’ve got ME”.  Whilst, in evidence before me, the Claimant protested that she would not have said that – but would rather have said: “I’ve had ME” – there was no challenge to the accuracy of the telephone conversation transcript.  
iii)	To have suffered hyponatraemia, the experts were agreed that the Claimant must have drunk very large, heroic amounts of water.  I have found that she did not vomit as much as suggested; but, to the extent that she did vomit, that would have reduced the amount of retained water in her body.  It is uncontroversial that the hyponatraemia was caused by psychogenic polydipsia: there was no physical cause for her thirst.  As Dr Isaac said in his evidence, psychogenic polydipsia is in itself a sign that all is not psychiatrically well.
iv)	Whilst it was common ground that a FLS could be present in a patient despite MRI scans showing no abnormalities, it was also common ground that changes to the brain that would be noticeable on an MRI scan would be expected in clinically significant FLS (paragraph 13 of the joint statement of the expert psychiatrists/psychologists dated 15-16 October 2015).  There were no such signs on successive MRI scans performed on the Claimant from 8 October 2009. 
v)	It was common ground that, in the Claimant’s case, there was (i) no brain stem herniation (coning), (ii) hypoxic ischaemic injury and (iii) osmotic demyelination.  Dr Howard’s evidence was that hyponatraemia absent these other conditions is incapable of causing brain damage, and there has never been a recorded case of it having done so.  I consider this evidence further below (paragraphs 158-161).
156.	Two area of the evidence warrants particular consideration.
157.	First, Dr Leng conducted a battery of neuropsychological test on the Claimant which, he said, if not diagnostic of FLS (his primary contention, considered above: see paragraph 152).  Dr Leng disagreed: but Mr Spencer submitted that, generally, Dr Leng was not a good witness, and to an extent I agree.  However, I also consider that Dr Leng over-played the test results he obtained.  As Mr Porter submitted, the results were, at their highest, a mixed bag.  The Claimant performed at high level (superior/high average) in the verbal fluency tests which, the neuropsychologists agreed, is an area often adversely affected in those who have suffered brain damage and particularly frontal lobe injury.  Her intellectual functions were normal (average); and her reading speed, selective attention, dividing attention, generally tests designed to test for emotional disorders and delayed memory index fell within the average (including low average) category.  Her immediate memory index was “very low level”, suggesting some deficit in laying down information in the memory; but the Claimant has denied memory problems in practice.  I accept that the Claimant did show some measured impairment in some of these results – in the sense that they were “low” average – and it is true that the score on the Cognitive Estimates Tests was abnormally low, but Dr Leng’s evidence was that these results do not by any means evince an obvious brain injury.  I agree with that.  I do not consider these result to be of great evidential weight.
158.	Second, there was a vigorous debate between Professor Chadwick and Dr Howard as to whether acute hyponatraemia is capable of causing generalised organic brain damage or selective frontal lobe damage, if it is unaccompanied by one of these conditions.  Dr Howard was firmly of the view that it could not, on the basis that there are no reported cases of it having thus occurred and no apparent mechanism for it doing so.  Professor Chadwick accepted that there was no known mechanism, or even a possible mechanism that he could suggest; but said (on page 8 of the preamble to the joint statement of experts dated 4 October 2015):
“… having considered the literature that it is possible to argue that acute hyponatraemia may be sufficient on its own to produce brain damage…”. 
159.	The literature to which he referred was restricted to a single substantive paper, namely Arieff AI, Hyponatraemia, convulsions, respiratory arrest, and permanent brain damage after elective surgery in healthy women, N Eng J Med, 1986. 314(24): 1529-35.  This paper considered fifteen cases where severe hyponatraemia developed after elective surgery in healthy women who subsequently died or suffered brain damage.  All patient are recorded as having woken from general anaesthesia, and being able to function for several hours after surgery, before suffering from grand mal seizures and, within an hour of the seizures starting, respiratory arrest.  All were intubated, but “had hypoxic-anoxic intervals of various durations” (page 1530).  All suffered organic brain damage.  This study has been used in at least one paper academically to support the proposition that organic brain damage may occur in those who suffer from hyponatraemia, without any of the other conditions to which I have referred (Sterns RH, Nigweker SU and Hix JK, The treatment of hyponatraemia. Semin Nephtol 2009. 29(3): 282-99); and in a standard text book (Angel MJ et al.  Handbook of Clinical Neurology. Vol 90 (3rd Series). Disorders of Consciousness.  Chapter 7: Metabolic encephalopathies at 136, citing (and only citing) the 1986 Arieff paper).  
160.	However, leaving aside Dr Howard’s concerns about the standard of reporting of these cases, in each of the fifteen case there was respiratory arrest.  Dr Howard considers that “it is inconceivable that these patients did not develop hypoxic-ischaemic brain injury particularly given the post-mortem findings [of characteristic cortical damage]” (page 10 of the preamble to the joint statement of experts dated 4 October 2015).  I find that evidence compelling.  Indeed, Arieff himself appears to have rejected the suggestion that brain damage can occur from hyponatraemia alone, attributing any long-term consequences of that condition to acute hypoxia (Arieff AI. Influence of hypoxic and sex on hyponatraemic encephalopathy.  Am Journal of Medicine 2006; 119; S59-S64).  
161.	In addition to the 1986 Arieff paper, Professor Chadwick relied upon three anecdotal cases from his clinical practice; but in Dr Howard’s view, to put it at its lowest, these are unconvincing, because of other potential explanations for the brain damage observed, namely herniation, hypoxia and osmotic demyelination respectively.  Dr Howard’s critique of this evidence, in my respectful view, had considerable force.
162.	Of course, in the circumstances of this case, I do not have to decide this issue determinatively.  Suffice it to say that, on the evidence before me, I find Dr Howard’s stance on this issue the more compelling      
163.	Overall, as I have made clear, I find the issue of medical causation particularly difficult; but, had I been required to determine the issue, I would have been persuaded by Mr Porter’s submissions: on the balance of probabilities, I consider that the Claimant does not suffer from an permanent organic brain injury.  
164.	In coming to that conclusion, I have taken into account all of the evidence – and particularly that to which I have referred above – but I find two factors of particular force, namely:
i)	The lack of any even suggested mechanism for hyponatraemia causing a frontal lobe injury, without one of the other conditions to which I refer above; and the evidence of Dr Howard as to the (in)capability of it doing so.
ii)	The Claimant’s pre-morbid medical history.  I have emphasised the importance of taking a balanced view with regard to this: but I was particularly impressed by the evidence of Dr Isaac, the psychiatrist instructed by the Defendants, on this point.  He gave his evidence in a particularly modest, balanced and (in my view) powerful way.  He accepted, readily, that the pattern of the Claimant’s symptoms would fit better with organic brain injury and FLS than with a somatic order; but for what he referred to as “the threads in the wind”, i.e. the generally comparable symptoms she had suffered previously, which suggests that she was psychologically vulnerable to this episode which, on any view, was a serious one.  In a case where medical causation is clearly very finely balanced, I found that evidence to be particularly persuasive.
165.	For those reasons, had I found the Defendants or either of them to have been in breach of duty, I would have found that the claim in any event failed because the Claimant has failed to prove that she has suffered organic brain damage as a result of the breach.
Capacity
166.	Given my findings on other issues, I can also deal with the Claimant’s capacity briefly.
167.	Section 2 of the Mental Health Capacity Act 2005 provides that a person lacks capacity in relation to a matter if, at the material time,  they are unable to make a decision for themselves in relation to the matter because of an impairment of, or a disturbance in the functioning of the mind or brain.  By section 1(2), a person must be assumed to have capacity unless it is established that he lacks capacity.  Therefore, the question whether a person lacks capacity within the meaning of this Act must be decided on the balance of probabilities, the burden of proof falling on the person who asserts that capacity is lacking.  
168.	The formula to be used in making the assessment as to whether the person concerned lacks the mental capacity to make a particular decision for themselves at the relevant time is set out in section 3 of the 2005 Act, which provides that a person is unable to make a decision for the purposes of section 2 if (amongst other things he is unable (a) to understand the information relevant to the decision, (b) to retain that information, and (c) to use or weigh that information as part of the process of making the decision.  By section 3(2), a person is not to be regarded as unable to understand the information relevant to a decision if he is able to understand an explanation of it given to him in a way that is appropriate to his circumstances.
169.	Mr Spencer, rightly, accepted that this was no stronger than a borderline case; but submitted that evidence in the Claimant’s case was sufficient to overcome the assumption of capacity.  He relied upon three main pieces of evidence:
i)	The Claimant’s history of withdrawal from household finances and financial management since her discharge from hospital in November 2009.
ii)	The evidence of Professor Chadwick that he thought she would be likely to exhibit impulsivity and so her ability to manage her financial affairs would be jeopardised.
iii)	Dr Shotbolt tested her in his assessment, by the use of an example.  She said that she would rather buy a £30 warranty for a washing machine to cover a month, than longer term alternatives.    
170.	These each go to the Claimant’s ability to make financial decisions.  The evidence in relation to her ability to conduct proceedings was even more limited.  Professor Chadwick said that he thought her ability to follow legal arguments would be greatly limited by her mental impairment.  Mr Lillington, on the other hand, was more positive.  He said that his wife found it difficult conceptually to understand the Bolam test – she is not unique in that – but he told Dr Shotbolt (the psychiatrist instructed by the Claimant) that he considered the Claimant did have both financial capacity and capacity to follow legal process (paragraph 4.16.5 of his report dated 20 May 2013).
171.	The only decision I have to take in relation to capacity is in relation to the these proceedings, no one having previously made any determination as to whether the Claimant has the capacity to have conducted them.  I have considered all of the evidence, including the above, and I am unpersuaded that this is a case in which the assumption of capacity in that regard has been overturned.  
Conclusion
172.	For those reasons, despite the more than able efforts of Mr Spencer and Ms Mangat, this claim is dismissed.